Fusarium head blight(FHB) caused by Fusarium graminearum is a devastating fungal disease on small grain cereal crops,because it reduces yield and quality and causes the mycotoxin contamination to the grain.Dynamins an...Fusarium head blight(FHB) caused by Fusarium graminearum is a devastating fungal disease on small grain cereal crops,because it reduces yield and quality and causes the mycotoxin contamination to the grain.Dynamins and dynamin-related proteins(DRPs) are large GTPase superfamily members,which are typically involved in the budding and division of vesicles in eukaryotic cells,but their roles in Fusarium spp.remain unexplored.Here,we found that FgDnm1,a DRP and homolog to Dnm1 in Saccharomyces cerevisiae,contributes to the normal fungal growth,sexual reproduction and sensitivity to fungicides.In addition,we found FgDnm1 co-localizes with mitochondria and is involved in toxisome formation and deoxynivalenol(DON) production.Several quinone outside inhibitors(QoIs) and succinate dehydrogenase inhibitors(SDHIs) cause fragmentated morphology of mitochondria.Importantly,the deletion of FgDnm1displays filamentous mitochondria and blocks the mitochondrial fragmentation induced by QoIs and SDHIs.Taken together,our studies uncover the effect of mitochondrial dynamics in fungal normal growth and how such events link to fungicides sensitivity and toxisome formation.Thus,we concluded that altered mitochondrial morphology induced by QoIs and SDHIs depends on FgDnm1.展开更多
BACKGROUND Mesenchymal stem cells(MSCs)are a type of stem cells that possess relevant regenerative abilities and can be used to treat many chronic diseases.Diabetes mellitus(DM)is a frequently diagnosed chronic diseas...BACKGROUND Mesenchymal stem cells(MSCs)are a type of stem cells that possess relevant regenerative abilities and can be used to treat many chronic diseases.Diabetes mellitus(DM)is a frequently diagnosed chronic disease characterized by hyperglycemia which initiates many multisystem complications in the long-run.DM patients can benefit from MSCs transplantation to curb down the pathological consequences associated with hyperglycemia persistence and restore the function of damaged tissues.MSCs therapeutic outcomes are found to last for short period of time and ultimately these regenerative cells are eradicated and died in DM disease model.AIM To investigate the impact of high glucose or hyperglycemia on the cellular and molecular characteristics of MSCs.METHODS Human adipose tissue-derived MSCs(hAD-MSCs)were seeded in low(5.6 mmol/L of glucose)and high glucose(25 mmol/L of glucose)for 7 d.Cytotoxicity,viability,mitochondrial dynamics,and apoptosis were deplored using specific kits.Western blotting was performed to measure the protein expression of phosphatidylinositol 3-kinase(PI3K),TSC1,and mammalian target of rapamycin(mTOR)in these cells.RESULTS hAD-MSCs cultured in high glucose for 7 d demonstrated marked decrease in their viability,as shown by a significant increase in lactate dehydrogenase(P<0.01)and a significant decrease in Trypan blue(P<0.05)in these cells compared to low glucose control.Mitochondrial membrane potential,indicated by tetramethylrhodamine ethyl ester(TMRE)fluorescence intensity,and nicotinamide adenine dinucleotide(NAD+)/NADH ratio were significantly dropped(P<0.05 for TMRE and P<0.01 for NAD+/NADH)in high glucose exposed hAD-MSCs,indicating disturbed mitochondrial function.PI3K protein expression significantly decreased in high glucose culture MSCs(P<0.05 compared to low glucose)and it was coupled with significant upregulation in TSC1(P<0.05)and downregulation in mTOR protein expression(P<0.05).Mitochondrial complexes I,IV,and V were downregulated profoundly in high glucose(P<0.05 compared to low glucose).Apoptosis was induced as a result of mitochondrial impairment and explained the poor survival of MSCs in high glucose.CONCLUSION High glucose impaired the mitochondrial dynamics and regulatory proteins in hAD-MSCs ensuing their poor survival and high apoptosis rate in hyperglycemic microenvironment.展开更多
Axonal regeneration in the central nervous system is an energy-intensive process.In contrast to mammals,adult zebrafish can functionally recover from neuronal injury.This raises the question of how zebrafish can cope ...Axonal regeneration in the central nervous system is an energy-intensive process.In contrast to mammals,adult zebrafish can functionally recover from neuronal injury.This raises the question of how zebrafish can cope with this high energy demand.We previously showed that in adult zebrafish,subjected to an optic nerve crush,an antagonistic axon-dendrite interplay exists wherein the retraction of retinal ganglion cell dendrites is a prerequisite for effective axonal repair.We postulate a‘dendrites for regeneration’paradigm that might be linked to intraneuronal mitochondrial reshuffling,as ganglion cells likely have insufficient resources to maintain dendrites and restore axons simultaneously.Here,we characterized both mitochondrial distribution and mitochondrial dynamics within the different ganglion cell compartments(dendrites,somas,and axons)during the regenerative process.Optic nerve crush resulted in a reduction of mitochondria in the dendrites during dendritic retraction,whereafter enlarged mitochondria appeared in the optic nerve/tract during axonal regrowth.Upon dendritic regrowth in the retina,mitochondrial density inside the retinal dendrites returned to baseline levels.Moreover,a transient increase in mitochondrial fission and biogenesis was observed in retinal ganglion cell somas after optic nerve damage.Taken together,these findings suggest that during optic nerve injury-induced regeneration,mitochondria shift from the dendrites to the axons and back again and that temporary changes in mitochondrial dynamics support axonal and dendritic regrowth after optic nerve crush.展开更多
Brown adipose tissue(BAT),crucial for mammalian thermoregulation and energy metabolism,boasts a dense concentration of mitochondria.As a vital cellular organelle,mitochondria undergo substantial remodeling in cold env...Brown adipose tissue(BAT),crucial for mammalian thermoregulation and energy metabolism,boasts a dense concentration of mitochondria.As a vital cellular organelle,mitochondria undergo substantial remodeling in cold environments,playing a pivotal role in maintaining body temperature and energy balance[1].Mitochondrial dynamics.展开更多
Background Increasing research suggests that mitochondrial defect plays a major role in pulmonary hypertension(PH) pathogenesis. Mitochondrial dynamics and quality control have a central role in the maintenance of the...Background Increasing research suggests that mitochondrial defect plays a major role in pulmonary hypertension(PH) pathogenesis. Mitochondrial dynamics and quality control have a central role in the maintenance of the cell proliferation and apoptosis balance. However, the molecular mechanism underlying of this balance is still unknown. Methods To clarify the biological effects of hypoxic air exposure and hypoxia-inducible factor-1α(HIF-1α) on pulmonary arterial smooth muscle cell(PASMC) and pulmonary arterial hypertension rats, the cells were cultured in a hypoxic chamber under oxygen concentrations. Cell viability, reactive oxygen species level, cell death, mitochondrial morphology, mitochondrial membrane potential, mitochondrial function and mitochondrial biosynthesis, as well as fission-and fusion-related proteins, were measured under hypoxic conditions. In addition, rats were maintained under hypoxic conditions, and the right ventricular systolic pressure, right ventricular hypertrophy index and right ventricular weight/body weight ratio were examined and recorded. Further, we assessed the role of HIF-1α in the development and progression of PH using HIF-1α gene knockdown using small interfering RNA transfection. Mdivi-1 treatment was performed before hypoxia to inhibit dynamin-related protein 1(Drp1). Results We found that HIF-1α expression was increased during hypoxia, which was crucial for hypoxia-induced mitochondrial dysfunction and hypoxia-stimulated PASMCs proliferation and apoptosis. We also found that targeting mitochondrial fission Drp1 by mitochondrial division inhibitor Mdivi-1 was effective in PH model rats. The results showed that mitochondrial dynamics were involved in the pulmonary vascular remodeling under hypoxia in vivo and in vitro. Furthermore, HIF-1α also modulated mitochondrial dynamics in pulmonary vascular remodeling under hypoxia through directly regulating the expression of Drp1. Conclusions In conclusion, our data suggests that abnormal mitochondrial dynamics could be a marker for the early diagnosis of PH and monitoring disease progression. Further research is needed to study the signaling pathways that govern mitochondrial fission/fusion in PH.展开更多
Impaired axonal development and degeneration underlie debilitating neurodegenerative diseases including hereditary spastic paraplegia, a large group of inherited diseases. Hereditary spastic paraplegia is caused by re...Impaired axonal development and degeneration underlie debilitating neurodegenerative diseases including hereditary spastic paraplegia, a large group of inherited diseases. Hereditary spastic paraplegia is caused by retrograde degeneration of the long corticospinal tract axons, leading to progressive spasticity and weakness of leg and hip muscles. There are over 70 subtypes with various underlying pathophysiological processes, such as defective vesicular trafficking, lipid metabolism, organelle shaping, axonal transport, and mitochondrial dysfunction. Although hereditary spastic paraplegia consists of various subtypes with different pathological characteristics, defects in mitochondrial morphology and function emerge as one of the common cellular themes in hereditary spastic paraplegia. Mitochondrial morphology and function are remodeled by mitochondrial dynamics regulated by several key fission and fusion mediators. However, the role of mitochondrial dynamics in axonal defects of hereditary spastic paraplegia remains largely unknown. Recently, studies reported perturbed mitochondrial morphology in hereditary spastic paraplegia neurons. Moreover, downregulation of mitochondrial fission regulator dynamin-related protein 1, both pharmacologically and genetically, could rescue axonal outgrowth defects in hereditary spastic paraplegia neurons, providing a potential therapeutic target for treating these hereditary spastic paraplegia. This mini-review will describe the regulation of mitochondrial fission/fusion, the link between mitochondrial dynamics and axonal defects, and the recent progress on the role of mitochondrial dynamics in axonal defects of hereditary spastic paraplegia.展开更多
Mitochondrial dysfunction is an early prominent feature in susceptible neurons in the brain of patients with Alzheimer′s disease which likely plays a critical role in the pathogenesis of disease. Mitochondria are dyn...Mitochondrial dysfunction is an early prominent feature in susceptible neurons in the brain of patients with Alzheimer′s disease which likely plays a critical role in the pathogenesis of disease. Mitochondria are dynamic organelles and the balance of mitochondrial fission and fusion determines Our initial studies revealed an imbalance in mitochondrial fission and fusion in fibroblasts from sporadic AD patients compared with normal healthy fibroblasts from age-matched control patients. Later it was demonstrated that overexpression of familial Alzheimer disease(FAD)-causing AβPP mutant or exposure to soluble Aβ oligomers led to mitochondrial fragmentation and redistribution in neuronal cells along with altered expression of mitochondrial fission/fusion proteins. Marked mitochondrial fragmentation and abnormal mitochondrial distribution in the pyramidal neurons along with mitochondrial dysfunction in the brain of AD mouse model CRND8 as early as three months of age before the accumulation of amyloid pathology. Importantly,we demonstrate significant changes in the expression and distribution of mitochondrial fission and fusion proteins in vivo in AD in consistent with a shifted mitochondrial dynamics towards excessive fission. Most recently,we demonstrated that genetic and pharmaceutical methods to rescue mitochondrial morphology and distribution could effectively restore Aβ-induced mitochondrial function and alleviate synaptic dysfunction both in vitro and in vivo,suggesting a causal involvement of mitochondrial dynamics in mediating Aβ-induced mitochondrial dysfunction. Taken together,we suggest that such a fundamental shift in mitochondrial dynamics negatively impacts all aspect of mitochondrial function such as impaired bioenergetics,increased structural damage and ROS production and loss of mt DNA integrity which causes synaptic dysfunction and neuronal dysfunction that is critical to AD pathogenesis. Therefore,strategies to modify abnormal mitochondrial dynamics may be an attractive therapeutic intervention target for AD.展开更多
<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increas...<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increased occurrence of atopic dermatitis, is now recognized, but its cellular mechanisms remain poorly understood. <strong>Objective:</strong> In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. We also sought to establish the protective effect of ECH-5195 (red <em>Panax ginseng</em> extract), standardized in ginsenosides, in reversing pollution-induced mitochondrial defects. <strong>Methods:</strong> Urban pollution exposure was mimicked by 1 h exposure of HaCaT cells with standardized atmospheric particulate matter containing PAHs, nitro-PAHs, PCB congeners, and chlorinated pesticides with a mean particulate diameter of 5.85 μm (SRM1648). <strong>Results:</strong> The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network. Pollution exposure was associated with a significant reduction of basal OCR and increased lactate production, pushing the cell to rely on glycolysis for ATP production. When ECH-5195 was used, OCR was significantly increased, and the glycolytic contribution to ATP production was reduced while both oxidative phosphorylation and mitochondrial respiration were increased demonstrating mitochondrial re-engagement in ATP production. <strong>Conclusions:</strong> Pollution exposure was disruptive for both the mitochondrial network dynamics and mitochondrial respiration. Ginsenosides in ECH-5195 efficiently protected both from pollution-induced defects.展开更多
Mitochondria undergo morphological changes during spermatogenesis in some animals.The mechanism and role of mitochondrial morphology regulation,however,remain somewhat unclear.In this study,we analyzed the molecular c...Mitochondria undergo morphological changes during spermatogenesis in some animals.The mechanism and role of mitochondrial morphology regulation,however,remain somewhat unclear.In this study,we analyzed the molecular characteristics,expression dynamics and subcellular localization of optic atrophy protein 1(OPA1),a mitochondrial fusion and cristae maintenance-related protein,to reveal the possible regulatory mechanisms underlying mitochondrial morphology in Phascolosoma esculenta spermiogenesis.The full-length cDNA of the P.esculenta opa1 gene(Pe-opa1)is 3743 bp in length and encodes 975 amino acids.The Pe-OPA1 protein is highly conservative and includes a transmembrane domain,a GTPase domain,two helical bundle domains,and a lipid-interacting stalk.Gene and protein expression was higher in the coelomic fluid(a site of spermatid development)of male P.esculenta and increased first and then decreased from March to December.Moreover,their expression during the breeding stage was significantly higher than during the non-breeding stage,suggesting that Pe-OPA1 is involved in P.esculenta reproduction.The Pe-OPA1 protein was more abundant in components consisting of many spermatids than in components without,indicating that Pe-OPA1 mainly plays a role in the spermatid in coelomic fluid.Moreover,Pe-OPA1 was mainly detected in the spermatid mitochondria.Immunofluorescence experiments showed that the Pe-OPA1 are constitutively expressed and co-localized with mitochondria during spermiogenesis,suggesting its involvement in P.esculenta spermiogenesis.These results provide evidence for Pe-OPA1's involvement in the regulation of mitochondrial morphology during spermiogenesis.展开更多
Optimal propagation of neuronal electrical impulses depends on the insulation of axons by myelin,produced in the central nervous system by oligodendrocytes.Myelin is an extension of the oligodendrocyte plasma membrane...Optimal propagation of neuronal electrical impulses depends on the insulation of axons by myelin,produced in the central nervous system by oligodendrocytes.Myelin is an extension of the oligodendrocyte plasma membrane,which wraps around an axon to form a compact multi-layered sheath.Myelin is composed of a substantially higher proportion of lipids compared to other biological membranes and enriched in a small number of specialized proteins.展开更多
Non-alcoholic fatty liver disease(NAFLD)is a chronic liver disease closely related to metabolic disorders that pose a serious threat to human health.Currently,no specific drugs are available for treating the aetiology...Non-alcoholic fatty liver disease(NAFLD)is a chronic liver disease closely related to metabolic disorders that pose a serious threat to human health.Currently,no specific drugs are available for treating the aetiology of NAFLD in clinical practice.Mitochondria have various biological functions inside the cell.Studies have found that mitochondrial fission and fusion are closely related to NAFLD.Therefore,identifying therapeutic targets for NAFLD through mitochondrial fission and fusion is crucial.Particularly in the field of traditional Chinese medicine,good therapeutic effects have been achieved in the treatment of NAFLD by protecting mitochondrial fusion and fission.Therefore,this article reviews the relationship between mitochondrial dynamics and NAFLD as well as the treatment of NAFLD through the regulation of mitochondrial fission and fusion with traditional Chinese medicine to provide a reference for the clinical application of traditional Chinese medicine in regulating mitochondrial fission and fusion functions to treat NAFLD.展开更多
Mitochondria play an essential role in neural function,such as supporting normal energy metabolism,regulating reactive oxygen species,buffering physiological calcium loads,and maintaining the balance of morphology,sub...Mitochondria play an essential role in neural function,such as supporting normal energy metabolism,regulating reactive oxygen species,buffering physiological calcium loads,and maintaining the balance of morphology,subcellular distribution,and overall health through mitochondrial dynamics.Given the recent technological advances in the assessment of mitochondrial structure and functions,mitochondrial dysfunction has been regarded as the early and key pathophysiological mechanism of cognitive disorders such as Alzheimer’s disease,Parkinson’s disease,Huntington’s disease,mild cognitive impairment,and postoperative cognitive dysfunction.This review will focus on the recent advances in mitochondrial medicine and research methodology in the field of cognitive sciences,from the perspectives of energy metabolism,oxidative stress,calcium homeostasis,and mitochondrial dynamics(including fission-fusion,transport,and mitophagy).展开更多
The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow.Mitochondria are directly affected by direct facto...The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow.Mitochondria are directly affected by direct factors such as ischemia,hypoxia,excitotoxicity,and toxicity of free hemoglobin and its degradation products,which trigger mitochondrial dysfunction.Dysfunctional mitochondria release large amounts of reactive oxygen species,inflammatory mediators,and apoptotic proteins that activate apoptotic pathways,further damaging cells.In response to this array of damage,cells have adopted multiple mitochondrial quality control mechanisms through evolution,including mitochondrial protein quality control,mitochondrial dynamics,mitophagy,mitochondrial biogenesis,and intercellular mitochondrial transfer,to maintain mitochondrial homeostasis under pathological conditions.Specific interventions targeting mitochondrial quality control mechanisms have emerged as promising therapeutic strategies for subarachnoid hemorrhage.This review provides an overview of recent research advances in mitochondrial pathophysiological processes after subarachnoid hemorrhage,particularly mitochondrial quality control mechanisms.It also presents potential therapeutic strategies to target mitochondrial quality control in subarachnoid hemorrhage.展开更多
Mitochondria are organelles that are able to adjust and respond to different stressors and metabolic needs within a cell,showcasing their plasticity and dynamic nature.These abilities allow them to effectively coordin...Mitochondria are organelles that are able to adjust and respond to different stressors and metabolic needs within a cell,showcasing their plasticity and dynamic nature.These abilities allow them to effectively coordinate various cellular functions.Mitochondrial dynamics refers to the changing process of fission,fusion,mitophagy and transport,which is crucial for optimal function in signal transduction and metabolism.An imbalance in mitochondrial dynamics can disrupt mitochondrial function,leading to abnormal cellular fate,and a range of diseases,including neurodegenerative disorders,metabolic diseases,cardiovascular diseases and cancers.Herein,we review the mechanism of mitochondrial dynamics,and its impacts on cellular function.We also delve into the changes that occur in mitochondrial dynamics during health and disease,and offer novel perspectives on how to target the modulation of mitochondrial dynamics.展开更多
With increasing population and changing demographics,food consumption has experienced a significant transition in quantity and quality.However,a dearth of knowledge remains regarding its environmental impacts and how ...With increasing population and changing demographics,food consumption has experienced a significant transition in quantity and quality.However,a dearth of knowledge remains regarding its environmental impacts and how it responds to demographic dynamics,particularly in emerging economies like China.Using the two-stage Quadratic Almost Demand System(QUAIDS)model,this study empirically examines the impact of demographic dynamics on food consumption and its environmental outcomes based on the provincial data from 2000 to 2020 in China.Under various scenarios,according to changes in demographics,we extend our analysis to project the long-term trend of food consumption and its environmental impacts,including greenhouse gas(GHG)emissions,water footprint(WF),and land appropriation(LA).The results reveal that an increase in the proportion of senior people significantly decreases the consumption of grain and livestock meat and increases the consumption of poultry,egg,and aquatic products,particularly for urban residents.Moreover,an increase in the proportion of males in the population leads to higher consumption of poultry and aquatic products.Correspondingly,in the current scenario of an increased aging population and sex ratio,it is anticipated that GHG emissions,WF,and LA are likely to decrease by 1.37,2.52,and 3.56%,respectively.More importantly,in the scenario adhering to the standards of nutritional intake according to the Dietary Guidelines for Chinese Residents in 2022,GHG emissions,WF,and LA in urban areas would increase by 12.78,20.94,and 18.32%,respectively.Our findings suggest that changing demographics should be considered when designing policies to mitigate the diet-environment-health trilemma and achieve sustainable food consumption.展开更多
With the integration of ultrafast reflectivity and polarimetry probes,we observed carrier relaxation and spin dynamics induced by ultrafast laser excitation of Ni(111)single crystals.The carrier relaxation time within...With the integration of ultrafast reflectivity and polarimetry probes,we observed carrier relaxation and spin dynamics induced by ultrafast laser excitation of Ni(111)single crystals.The carrier relaxation time within the linear excitation range reveals that electron-phonon coupling and dissipation of photon energy into the bulk of the crystal take tens of picoseconds.On the other hand,the observed spin dynamics indicate a longer time of about 120 ps.To further understand how the lattice degree of freedom is coupled with these dynamics may require the integration of an ultrafast diffraction probe.展开更多
This paper presents a mathematical model consisting of conservation and balance laws (CBL) of classical continuum mechanics (CCM) and ordered rate constitutive theories in Lagrangian description derived using entropy ...This paper presents a mathematical model consisting of conservation and balance laws (CBL) of classical continuum mechanics (CCM) and ordered rate constitutive theories in Lagrangian description derived using entropy inequality and the representation theorem for thermoviscoelastic solids (TVES) with rheology. The CBL and the constitutive theories take into account finite deformation and finite strain deformation physics and are based on contravariant deviatoric second Piola-Kirchhoff stress tensor and its work conjugate covariant Green’s strain tensor and their material derivatives of up to order m and n respectively. All published works on nonlinear dynamics of TVES with rheology are mostly based on phenomenological mathematical models. In rare instances, some aspects of CBL are used but are incorrectly altered to obtain mass, stiffness and damping matrices using space-time decoupled approaches. In the work presented in this paper, we show that this is not possible using CBL of CCM for TVES with rheology. Thus, the mathematical models used currently in the published works are not the correct description of the physics of nonlinear dynamics of TVES with rheology. The mathematical model used in the present work is strictly based on the CBL of CCM and is thermodynamically and mathematically consistent and the space-time coupled finite element methodology used in this work is unconditionally stable and provides solutions with desired accuracy and is ideally suited for nonlinear dynamics of TVES with memory. The work in this paper is the first presentation of a mathematical model strictly based on CBL of CCM and the solution of the mathematical model is obtained using unconditionally stable space-time coupled computational methodology that provides control over the errors in the evolution. Both space-time coupled and space-time decoupled finite element formulations are considered for obtaining solutions of the IVPs described by the mathematical model and are presented in the paper. Factors or the physics influencing dynamic response and dynamic bifurcation for TVES with rheology are identified and are also demonstrated through model problem studies. A simple model problem consisting of a rod (1D) of TVES material with memory fixed at one end and subjected to harmonic excitation at the other end is considered to study nonlinear dynamics of TVES with rheology, frequency response as well as dynamic bifurcation phenomenon.展开更多
BACKGROUND The precise role of mitochondrial carrier homolog 2(MTCH2)in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated.AIM To determi...BACKGROUND The precise role of mitochondrial carrier homolog 2(MTCH2)in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated.AIM To determine the role of MTCH2 in gastric cancer.METHODS We collected 65 samples of poorly differentiated gastric cancer tissue and adjacent tissues,constructed MTCH2-overexpressing and MTCH2-knockdown cell models,and evaluated the proliferation,migration,and invasion of human gastric epithelial cells(GES-1)and human gastric cancer cells(AGS)cells.The mito-chondrial membrane potential(MMP),mitochondrial permeability transformation pore(mPTP)and ATP fluorescence probe were used to detect mitochondrial function.Mitochondrial function and ATP synthase protein levels were detected via Western blotting.RESULTS The expression of MTCH2 and ATP2A2 in gastric cancer tissues was significantly greater than that in adjacent tissues.Overexpression of MTCH2 promoted colony formation,invasion,migration,MMP expression and ATP production in GES-1 and AGS cells while upregulating ATP2A2 expression and inhibiting cell apoptosis;knockdown of MTCH2 had the opposite effect,promoting overactivation of the mPTP and promoting apoptosis.CONCLUSION MTCH2 can increase the malignant phenotype of GES-1 cells and promote the proliferation,invasion,and migration of gastric cancer cells by regulating mitochondrial function,providing a basis for targeted therapy for gastric cancer cells.展开更多
Resveratrol(RSV),as a functional food component extracted from natural plants,has been widely studied and recognized in preventing and treating various diseases,with major mechanisms including executing anti-inflammat...Resveratrol(RSV),as a functional food component extracted from natural plants,has been widely studied and recognized in preventing and treating various diseases,with major mechanisms including executing anti-inflammation and anti-oxidation functions,and improving mitochondrial quality.Chronic diseases as non-communicable diseases are mainly caused by multiple factors,such as physiological decline and dysfunction in the body,and have become a significant challenge on public health worldwide.It is worth noting that chronic diseases such as Alzheimer's disease(AD),Parkinson's disease(PD),muscle atrophy,cardiovascular disease,obesity,and cancer are accompanied by abnormal mitochondrial function.Therefore,targeted regulation of mitochondria may be a meaningful way to prevent and treat chronic diseases.Increasing evidence has confirmed that RSV is actively involved in regulating mitochondria,and it has become an essential consideration to prevent and treat chronic diseases through targeting mitochondria and improving corresponding functions.In this article,current studies on RSV to optimize mitochondrial quality for preventing and alleviating chronic disease are systematically summarized,which can provide a theoretical reference for the development of functional foods or drugs to combat chronic diseases.展开更多
Objective Keshan disease(KD)is a myocardial mitochondrial disease closely related to insufficient selenium(Se)and protein intake.PTEN induced putative kinase 1(PINK1)/Parkin mediated mitochondrial autophagy regulates ...Objective Keshan disease(KD)is a myocardial mitochondrial disease closely related to insufficient selenium(Se)and protein intake.PTEN induced putative kinase 1(PINK1)/Parkin mediated mitochondrial autophagy regulates various physiological and pathological processes in the body.This study aimed to elucidate the relationship between PINK1/Parkin-regulated mitochondrial autophagy and KD-related myocardial injury.Methods A low Se and low protein animal model was established.One hundred Wistar rats were randomly divided into 5 groups(control group,low Se group,low protein group,low Se+low protein group,and corn from KD area group).The JC-1 method was used to detect the mitochondrial membrane potential(MMP).ELISA was used to detect serum creatine kinase MB(CK-MB),cardiac troponin I(cTnI),and mitochondrial-glutamicoxalacetic transaminase(M-GOT)levels.RT-PCR and Western blot analysis were used to detect the expression of PINK1,Parkin,sequestome 1(P62),and microtubule-associated proteins1A/1B light chain 3B(MAP1LC3B).Results The MMP was significantly decreased and the activity of CK-MB,cTnI,and M-GOT significantly increased in each experimental group(low Se group,low protein group,low Se+low protein group and corn from KD area group)compared with the control group(P<0.05 for all).The mRNA and protein expression levels of PINK1,Parkin and MAP1LC3B were profoundly increased,and those of P62 markedly decreased in the experimental groups compared with the control group(P<0.05 for all).Conclusion Low Se and low protein levels exacerbate myocardial damage in KD by affecting the PINK1/Parkin-mediated mitochondrial autophagy pathway.展开更多
基金supported by the National Natural Science Foundation of China (31772190)the Jiangsu Agriculture Science and Technology Innovation Fund, China (JASTIF) (CX(21)2037)the Postgraduate Research & Practice Innovation Program of Jiangsu Province, China (KYCX21_0631)。
文摘Fusarium head blight(FHB) caused by Fusarium graminearum is a devastating fungal disease on small grain cereal crops,because it reduces yield and quality and causes the mycotoxin contamination to the grain.Dynamins and dynamin-related proteins(DRPs) are large GTPase superfamily members,which are typically involved in the budding and division of vesicles in eukaryotic cells,but their roles in Fusarium spp.remain unexplored.Here,we found that FgDnm1,a DRP and homolog to Dnm1 in Saccharomyces cerevisiae,contributes to the normal fungal growth,sexual reproduction and sensitivity to fungicides.In addition,we found FgDnm1 co-localizes with mitochondria and is involved in toxisome formation and deoxynivalenol(DON) production.Several quinone outside inhibitors(QoIs) and succinate dehydrogenase inhibitors(SDHIs) cause fragmentated morphology of mitochondria.Importantly,the deletion of FgDnm1displays filamentous mitochondria and blocks the mitochondrial fragmentation induced by QoIs and SDHIs.Taken together,our studies uncover the effect of mitochondrial dynamics in fungal normal growth and how such events link to fungicides sensitivity and toxisome formation.Thus,we concluded that altered mitochondrial morphology induced by QoIs and SDHIs depends on FgDnm1.
文摘BACKGROUND Mesenchymal stem cells(MSCs)are a type of stem cells that possess relevant regenerative abilities and can be used to treat many chronic diseases.Diabetes mellitus(DM)is a frequently diagnosed chronic disease characterized by hyperglycemia which initiates many multisystem complications in the long-run.DM patients can benefit from MSCs transplantation to curb down the pathological consequences associated with hyperglycemia persistence and restore the function of damaged tissues.MSCs therapeutic outcomes are found to last for short period of time and ultimately these regenerative cells are eradicated and died in DM disease model.AIM To investigate the impact of high glucose or hyperglycemia on the cellular and molecular characteristics of MSCs.METHODS Human adipose tissue-derived MSCs(hAD-MSCs)were seeded in low(5.6 mmol/L of glucose)and high glucose(25 mmol/L of glucose)for 7 d.Cytotoxicity,viability,mitochondrial dynamics,and apoptosis were deplored using specific kits.Western blotting was performed to measure the protein expression of phosphatidylinositol 3-kinase(PI3K),TSC1,and mammalian target of rapamycin(mTOR)in these cells.RESULTS hAD-MSCs cultured in high glucose for 7 d demonstrated marked decrease in their viability,as shown by a significant increase in lactate dehydrogenase(P<0.01)and a significant decrease in Trypan blue(P<0.05)in these cells compared to low glucose control.Mitochondrial membrane potential,indicated by tetramethylrhodamine ethyl ester(TMRE)fluorescence intensity,and nicotinamide adenine dinucleotide(NAD+)/NADH ratio were significantly dropped(P<0.05 for TMRE and P<0.01 for NAD+/NADH)in high glucose exposed hAD-MSCs,indicating disturbed mitochondrial function.PI3K protein expression significantly decreased in high glucose culture MSCs(P<0.05 compared to low glucose)and it was coupled with significant upregulation in TSC1(P<0.05)and downregulation in mTOR protein expression(P<0.05).Mitochondrial complexes I,IV,and V were downregulated profoundly in high glucose(P<0.05 compared to low glucose).Apoptosis was induced as a result of mitochondrial impairment and explained the poor survival of MSCs in high glucose.CONCLUSION High glucose impaired the mitochondrial dynamics and regulatory proteins in hAD-MSCs ensuing their poor survival and high apoptosis rate in hyperglycemic microenvironment.
基金financially supported by the Katholieke Universiteit Leuven Research Council (C14/18/053)the research foundation Flanders (FWO) (G082221N)+1 种基金a personal L’Oréal/UNESCO (For Women in Science) fellowshipa personal FWO fellowship
文摘Axonal regeneration in the central nervous system is an energy-intensive process.In contrast to mammals,adult zebrafish can functionally recover from neuronal injury.This raises the question of how zebrafish can cope with this high energy demand.We previously showed that in adult zebrafish,subjected to an optic nerve crush,an antagonistic axon-dendrite interplay exists wherein the retraction of retinal ganglion cell dendrites is a prerequisite for effective axonal repair.We postulate a‘dendrites for regeneration’paradigm that might be linked to intraneuronal mitochondrial reshuffling,as ganglion cells likely have insufficient resources to maintain dendrites and restore axons simultaneously.Here,we characterized both mitochondrial distribution and mitochondrial dynamics within the different ganglion cell compartments(dendrites,somas,and axons)during the regenerative process.Optic nerve crush resulted in a reduction of mitochondria in the dendrites during dendritic retraction,whereafter enlarged mitochondria appeared in the optic nerve/tract during axonal regrowth.Upon dendritic regrowth in the retina,mitochondrial density inside the retinal dendrites returned to baseline levels.Moreover,a transient increase in mitochondrial fission and biogenesis was observed in retinal ganglion cell somas after optic nerve damage.Taken together,these findings suggest that during optic nerve injury-induced regeneration,mitochondria shift from the dendrites to the axons and back again and that temporary changes in mitochondrial dynamics support axonal and dendritic regrowth after optic nerve crush.
基金This study was financially supported by the National Natural Science Foundation of China(No.82270396).
文摘Brown adipose tissue(BAT),crucial for mammalian thermoregulation and energy metabolism,boasts a dense concentration of mitochondria.As a vital cellular organelle,mitochondria undergo substantial remodeling in cold environments,playing a pivotal role in maintaining body temperature and energy balance[1].Mitochondrial dynamics.
基金supported by the National Natural Science Foundation of China (No. 81673858, No. 81704062, No. 30500644)the Science and Technology Project of Traditional Chinese Medicine in Hunan (No. 2009045, No. 2012027)the Program for National Center for Clinical Medicine for Geriatric Diseases (Ministry of Science and Technology)
文摘Background Increasing research suggests that mitochondrial defect plays a major role in pulmonary hypertension(PH) pathogenesis. Mitochondrial dynamics and quality control have a central role in the maintenance of the cell proliferation and apoptosis balance. However, the molecular mechanism underlying of this balance is still unknown. Methods To clarify the biological effects of hypoxic air exposure and hypoxia-inducible factor-1α(HIF-1α) on pulmonary arterial smooth muscle cell(PASMC) and pulmonary arterial hypertension rats, the cells were cultured in a hypoxic chamber under oxygen concentrations. Cell viability, reactive oxygen species level, cell death, mitochondrial morphology, mitochondrial membrane potential, mitochondrial function and mitochondrial biosynthesis, as well as fission-and fusion-related proteins, were measured under hypoxic conditions. In addition, rats were maintained under hypoxic conditions, and the right ventricular systolic pressure, right ventricular hypertrophy index and right ventricular weight/body weight ratio were examined and recorded. Further, we assessed the role of HIF-1α in the development and progression of PH using HIF-1α gene knockdown using small interfering RNA transfection. Mdivi-1 treatment was performed before hypoxia to inhibit dynamin-related protein 1(Drp1). Results We found that HIF-1α expression was increased during hypoxia, which was crucial for hypoxia-induced mitochondrial dysfunction and hypoxia-stimulated PASMCs proliferation and apoptosis. We also found that targeting mitochondrial fission Drp1 by mitochondrial division inhibitor Mdivi-1 was effective in PH model rats. The results showed that mitochondrial dynamics were involved in the pulmonary vascular remodeling under hypoxia in vivo and in vitro. Furthermore, HIF-1α also modulated mitochondrial dynamics in pulmonary vascular remodeling under hypoxia through directly regulating the expression of Drp1. Conclusions In conclusion, our data suggests that abnormal mitochondrial dynamics could be a marker for the early diagnosis of PH and monitoring disease progression. Further research is needed to study the signaling pathways that govern mitochondrial fission/fusion in PH.
文摘Impaired axonal development and degeneration underlie debilitating neurodegenerative diseases including hereditary spastic paraplegia, a large group of inherited diseases. Hereditary spastic paraplegia is caused by retrograde degeneration of the long corticospinal tract axons, leading to progressive spasticity and weakness of leg and hip muscles. There are over 70 subtypes with various underlying pathophysiological processes, such as defective vesicular trafficking, lipid metabolism, organelle shaping, axonal transport, and mitochondrial dysfunction. Although hereditary spastic paraplegia consists of various subtypes with different pathological characteristics, defects in mitochondrial morphology and function emerge as one of the common cellular themes in hereditary spastic paraplegia. Mitochondrial morphology and function are remodeled by mitochondrial dynamics regulated by several key fission and fusion mediators. However, the role of mitochondrial dynamics in axonal defects of hereditary spastic paraplegia remains largely unknown. Recently, studies reported perturbed mitochondrial morphology in hereditary spastic paraplegia neurons. Moreover, downregulation of mitochondrial fission regulator dynamin-related protein 1, both pharmacologically and genetically, could rescue axonal outgrowth defects in hereditary spastic paraplegia neurons, providing a potential therapeutic target for treating these hereditary spastic paraplegia. This mini-review will describe the regulation of mitochondrial fission/fusion, the link between mitochondrial dynamics and axonal defects, and the recent progress on the role of mitochondrial dynamics in axonal defects of hereditary spastic paraplegia.
文摘Mitochondrial dysfunction is an early prominent feature in susceptible neurons in the brain of patients with Alzheimer′s disease which likely plays a critical role in the pathogenesis of disease. Mitochondria are dynamic organelles and the balance of mitochondrial fission and fusion determines Our initial studies revealed an imbalance in mitochondrial fission and fusion in fibroblasts from sporadic AD patients compared with normal healthy fibroblasts from age-matched control patients. Later it was demonstrated that overexpression of familial Alzheimer disease(FAD)-causing AβPP mutant or exposure to soluble Aβ oligomers led to mitochondrial fragmentation and redistribution in neuronal cells along with altered expression of mitochondrial fission/fusion proteins. Marked mitochondrial fragmentation and abnormal mitochondrial distribution in the pyramidal neurons along with mitochondrial dysfunction in the brain of AD mouse model CRND8 as early as three months of age before the accumulation of amyloid pathology. Importantly,we demonstrate significant changes in the expression and distribution of mitochondrial fission and fusion proteins in vivo in AD in consistent with a shifted mitochondrial dynamics towards excessive fission. Most recently,we demonstrated that genetic and pharmaceutical methods to rescue mitochondrial morphology and distribution could effectively restore Aβ-induced mitochondrial function and alleviate synaptic dysfunction both in vitro and in vivo,suggesting a causal involvement of mitochondrial dynamics in mediating Aβ-induced mitochondrial dysfunction. Taken together,we suggest that such a fundamental shift in mitochondrial dynamics negatively impacts all aspect of mitochondrial function such as impaired bioenergetics,increased structural damage and ROS production and loss of mt DNA integrity which causes synaptic dysfunction and neuronal dysfunction that is critical to AD pathogenesis. Therefore,strategies to modify abnormal mitochondrial dynamics may be an attractive therapeutic intervention target for AD.
文摘<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increased occurrence of atopic dermatitis, is now recognized, but its cellular mechanisms remain poorly understood. <strong>Objective:</strong> In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. We also sought to establish the protective effect of ECH-5195 (red <em>Panax ginseng</em> extract), standardized in ginsenosides, in reversing pollution-induced mitochondrial defects. <strong>Methods:</strong> Urban pollution exposure was mimicked by 1 h exposure of HaCaT cells with standardized atmospheric particulate matter containing PAHs, nitro-PAHs, PCB congeners, and chlorinated pesticides with a mean particulate diameter of 5.85 μm (SRM1648). <strong>Results:</strong> The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network. Pollution exposure was associated with a significant reduction of basal OCR and increased lactate production, pushing the cell to rely on glycolysis for ATP production. When ECH-5195 was used, OCR was significantly increased, and the glycolytic contribution to ATP production was reduced while both oxidative phosphorylation and mitochondrial respiration were increased demonstrating mitochondrial re-engagement in ATP production. <strong>Conclusions:</strong> Pollution exposure was disruptive for both the mitochondrial network dynamics and mitochondrial respiration. Ginsenosides in ECH-5195 efficiently protected both from pollution-induced defects.
基金the Ningbo Science and Technology Plan Projects(Nos.2019B10016,2016C10004)the Major Science and Technology Projects in Zhejiang Province(No.2011C12013)+1 种基金the Natural Science Foundation of Zhejiang Province(No.LY18C190007)the Collaborative Innovation Center for Zhejiang Marine High-efficiency and Healthy Aquaculture,the K.C.Wong Magna Fund in Ningbo University。
文摘Mitochondria undergo morphological changes during spermatogenesis in some animals.The mechanism and role of mitochondrial morphology regulation,however,remain somewhat unclear.In this study,we analyzed the molecular characteristics,expression dynamics and subcellular localization of optic atrophy protein 1(OPA1),a mitochondrial fusion and cristae maintenance-related protein,to reveal the possible regulatory mechanisms underlying mitochondrial morphology in Phascolosoma esculenta spermiogenesis.The full-length cDNA of the P.esculenta opa1 gene(Pe-opa1)is 3743 bp in length and encodes 975 amino acids.The Pe-OPA1 protein is highly conservative and includes a transmembrane domain,a GTPase domain,two helical bundle domains,and a lipid-interacting stalk.Gene and protein expression was higher in the coelomic fluid(a site of spermatid development)of male P.esculenta and increased first and then decreased from March to December.Moreover,their expression during the breeding stage was significantly higher than during the non-breeding stage,suggesting that Pe-OPA1 is involved in P.esculenta reproduction.The Pe-OPA1 protein was more abundant in components consisting of many spermatids than in components without,indicating that Pe-OPA1 mainly plays a role in the spermatid in coelomic fluid.Moreover,Pe-OPA1 was mainly detected in the spermatid mitochondria.Immunofluorescence experiments showed that the Pe-OPA1 are constitutively expressed and co-localized with mitochondria during spermiogenesis,suggesting its involvement in P.esculenta spermiogenesis.These results provide evidence for Pe-OPA1's involvement in the regulation of mitochondrial morphology during spermiogenesis.
基金supported by on operating grant(#1038154) from the Multiple Sclerosis Society of Canada (to TEK)a Multiple Sclerosis Society of Canada Post-Doctoral Fellowship (to JDMG)。
文摘Optimal propagation of neuronal electrical impulses depends on the insulation of axons by myelin,produced in the central nervous system by oligodendrocytes.Myelin is an extension of the oligodendrocyte plasma membrane,which wraps around an axon to form a compact multi-layered sheath.Myelin is composed of a substantially higher proportion of lipids compared to other biological membranes and enriched in a small number of specialized proteins.
文摘Non-alcoholic fatty liver disease(NAFLD)is a chronic liver disease closely related to metabolic disorders that pose a serious threat to human health.Currently,no specific drugs are available for treating the aetiology of NAFLD in clinical practice.Mitochondria have various biological functions inside the cell.Studies have found that mitochondrial fission and fusion are closely related to NAFLD.Therefore,identifying therapeutic targets for NAFLD through mitochondrial fission and fusion is crucial.Particularly in the field of traditional Chinese medicine,good therapeutic effects have been achieved in the treatment of NAFLD by protecting mitochondrial fusion and fission.Therefore,this article reviews the relationship between mitochondrial dynamics and NAFLD as well as the treatment of NAFLD through the regulation of mitochondrial fission and fusion with traditional Chinese medicine to provide a reference for the clinical application of traditional Chinese medicine in regulating mitochondrial fission and fusion functions to treat NAFLD.
基金supported by the National Natural Science Foundation of China,Nos.82271222(to ZL),81971012(to ZL),82071189(to XG),and 82201335(to YL)Key Clinical Projects of Peking University Third Hospital,No.BYSYZD2019027(to ZL)。
文摘Mitochondria play an essential role in neural function,such as supporting normal energy metabolism,regulating reactive oxygen species,buffering physiological calcium loads,and maintaining the balance of morphology,subcellular distribution,and overall health through mitochondrial dynamics.Given the recent technological advances in the assessment of mitochondrial structure and functions,mitochondrial dysfunction has been regarded as the early and key pathophysiological mechanism of cognitive disorders such as Alzheimer’s disease,Parkinson’s disease,Huntington’s disease,mild cognitive impairment,and postoperative cognitive dysfunction.This review will focus on the recent advances in mitochondrial medicine and research methodology in the field of cognitive sciences,from the perspectives of energy metabolism,oxidative stress,calcium homeostasis,and mitochondrial dynamics(including fission-fusion,transport,and mitophagy).
基金supported by the National Natural Science Foundation of China,Nos.82130037(to CH),81971122(to CH),82171323(to WL)the Natural Science Foundation of Jiangsu Province of China,No.BK20201113(to WL)。
文摘The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow.Mitochondria are directly affected by direct factors such as ischemia,hypoxia,excitotoxicity,and toxicity of free hemoglobin and its degradation products,which trigger mitochondrial dysfunction.Dysfunctional mitochondria release large amounts of reactive oxygen species,inflammatory mediators,and apoptotic proteins that activate apoptotic pathways,further damaging cells.In response to this array of damage,cells have adopted multiple mitochondrial quality control mechanisms through evolution,including mitochondrial protein quality control,mitochondrial dynamics,mitophagy,mitochondrial biogenesis,and intercellular mitochondrial transfer,to maintain mitochondrial homeostasis under pathological conditions.Specific interventions targeting mitochondrial quality control mechanisms have emerged as promising therapeutic strategies for subarachnoid hemorrhage.This review provides an overview of recent research advances in mitochondrial pathophysiological processes after subarachnoid hemorrhage,particularly mitochondrial quality control mechanisms.It also presents potential therapeutic strategies to target mitochondrial quality control in subarachnoid hemorrhage.
基金This work was supported by the NSFC of China(No.82273212 to H.Z.)the Major International(Regional)Joint Research Program of the NSFC of China(No.81920108027 to Y.L.)+1 种基金Performance Incentive for Scientific Research Institutions of Chongqing Guide Special Projects(No.cstc2020jxjl130014 to H.Z.)Research and Breeding Project of Chongqing Medical Biotechnology Association(No.cmba2022kyym-zkxmQ0006 to H.Z.).
文摘Mitochondria are organelles that are able to adjust and respond to different stressors and metabolic needs within a cell,showcasing their plasticity and dynamic nature.These abilities allow them to effectively coordinate various cellular functions.Mitochondrial dynamics refers to the changing process of fission,fusion,mitophagy and transport,which is crucial for optimal function in signal transduction and metabolism.An imbalance in mitochondrial dynamics can disrupt mitochondrial function,leading to abnormal cellular fate,and a range of diseases,including neurodegenerative disorders,metabolic diseases,cardiovascular diseases and cancers.Herein,we review the mechanism of mitochondrial dynamics,and its impacts on cellular function.We also delve into the changes that occur in mitochondrial dynamics during health and disease,and offer novel perspectives on how to target the modulation of mitochondrial dynamics.
基金This work was supported by the Qinchuangyuan Project of Shaanxi Province,China(QCYRCXM-2022-145)the Major Project of the Key Research Base of Humanities and Social Sciences of the Ministry of Education,China(22JJD790052)+1 种基金the Chinese Universities Scientific Fund(Z1010422003)the National Natural Science Foundation of China(72373117).
文摘With increasing population and changing demographics,food consumption has experienced a significant transition in quantity and quality.However,a dearth of knowledge remains regarding its environmental impacts and how it responds to demographic dynamics,particularly in emerging economies like China.Using the two-stage Quadratic Almost Demand System(QUAIDS)model,this study empirically examines the impact of demographic dynamics on food consumption and its environmental outcomes based on the provincial data from 2000 to 2020 in China.Under various scenarios,according to changes in demographics,we extend our analysis to project the long-term trend of food consumption and its environmental impacts,including greenhouse gas(GHG)emissions,water footprint(WF),and land appropriation(LA).The results reveal that an increase in the proportion of senior people significantly decreases the consumption of grain and livestock meat and increases the consumption of poultry,egg,and aquatic products,particularly for urban residents.Moreover,an increase in the proportion of males in the population leads to higher consumption of poultry and aquatic products.Correspondingly,in the current scenario of an increased aging population and sex ratio,it is anticipated that GHG emissions,WF,and LA are likely to decrease by 1.37,2.52,and 3.56%,respectively.More importantly,in the scenario adhering to the standards of nutritional intake according to the Dietary Guidelines for Chinese Residents in 2022,GHG emissions,WF,and LA in urban areas would increase by 12.78,20.94,and 18.32%,respectively.Our findings suggest that changing demographics should be considered when designing policies to mitigate the diet-environment-health trilemma and achieve sustainable food consumption.
基金Project supported by the National Key R&D Program of China (Grant Nos. 2022YFA1604402 and 2022YFA1604403)the National Natural Science Foundation of China (NSFC) (Grant No. 11721404)+3 种基金the Shanghai Rising-Star Program (Grant No. 21QA1406100)the Technology Innovation Action Plan of the Science and Technology Commission of Shanghai Municipality (Grant No. 20JC1416000)support by the Air Force Office of Scientific Research (AFOSR) (Grant No. FA9550-20-10139)the Texas A&M Engineering Experimental Station (TEES)
文摘With the integration of ultrafast reflectivity and polarimetry probes,we observed carrier relaxation and spin dynamics induced by ultrafast laser excitation of Ni(111)single crystals.The carrier relaxation time within the linear excitation range reveals that electron-phonon coupling and dissipation of photon energy into the bulk of the crystal take tens of picoseconds.On the other hand,the observed spin dynamics indicate a longer time of about 120 ps.To further understand how the lattice degree of freedom is coupled with these dynamics may require the integration of an ultrafast diffraction probe.
文摘This paper presents a mathematical model consisting of conservation and balance laws (CBL) of classical continuum mechanics (CCM) and ordered rate constitutive theories in Lagrangian description derived using entropy inequality and the representation theorem for thermoviscoelastic solids (TVES) with rheology. The CBL and the constitutive theories take into account finite deformation and finite strain deformation physics and are based on contravariant deviatoric second Piola-Kirchhoff stress tensor and its work conjugate covariant Green’s strain tensor and their material derivatives of up to order m and n respectively. All published works on nonlinear dynamics of TVES with rheology are mostly based on phenomenological mathematical models. In rare instances, some aspects of CBL are used but are incorrectly altered to obtain mass, stiffness and damping matrices using space-time decoupled approaches. In the work presented in this paper, we show that this is not possible using CBL of CCM for TVES with rheology. Thus, the mathematical models used currently in the published works are not the correct description of the physics of nonlinear dynamics of TVES with rheology. The mathematical model used in the present work is strictly based on the CBL of CCM and is thermodynamically and mathematically consistent and the space-time coupled finite element methodology used in this work is unconditionally stable and provides solutions with desired accuracy and is ideally suited for nonlinear dynamics of TVES with memory. The work in this paper is the first presentation of a mathematical model strictly based on CBL of CCM and the solution of the mathematical model is obtained using unconditionally stable space-time coupled computational methodology that provides control over the errors in the evolution. Both space-time coupled and space-time decoupled finite element formulations are considered for obtaining solutions of the IVPs described by the mathematical model and are presented in the paper. Factors or the physics influencing dynamic response and dynamic bifurcation for TVES with rheology are identified and are also demonstrated through model problem studies. A simple model problem consisting of a rod (1D) of TVES material with memory fixed at one end and subjected to harmonic excitation at the other end is considered to study nonlinear dynamics of TVES with rheology, frequency response as well as dynamic bifurcation phenomenon.
基金the Medical Science Research Projects in Hebei Province,No.20221526and Natural Science Foundation,No.2022-271.
文摘BACKGROUND The precise role of mitochondrial carrier homolog 2(MTCH2)in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated.AIM To determine the role of MTCH2 in gastric cancer.METHODS We collected 65 samples of poorly differentiated gastric cancer tissue and adjacent tissues,constructed MTCH2-overexpressing and MTCH2-knockdown cell models,and evaluated the proliferation,migration,and invasion of human gastric epithelial cells(GES-1)and human gastric cancer cells(AGS)cells.The mito-chondrial membrane potential(MMP),mitochondrial permeability transformation pore(mPTP)and ATP fluorescence probe were used to detect mitochondrial function.Mitochondrial function and ATP synthase protein levels were detected via Western blotting.RESULTS The expression of MTCH2 and ATP2A2 in gastric cancer tissues was significantly greater than that in adjacent tissues.Overexpression of MTCH2 promoted colony formation,invasion,migration,MMP expression and ATP production in GES-1 and AGS cells while upregulating ATP2A2 expression and inhibiting cell apoptosis;knockdown of MTCH2 had the opposite effect,promoting overactivation of the mPTP and promoting apoptosis.CONCLUSION MTCH2 can increase the malignant phenotype of GES-1 cells and promote the proliferation,invasion,and migration of gastric cancer cells by regulating mitochondrial function,providing a basis for targeted therapy for gastric cancer cells.
基金supported by the National Natural Science Foundation of China(No.32071176)the 14th Five-Year-Plan Advantageous and Characteristic Disciplines(Groups)of Colleges and Universities in Hubei Province for Exercise and Brain Science from Hubei Provincial Department of Education+1 种基金the Chutian Scholar ProgramInnovative Start-Up Foundation from Wuhan Sports University to Ning Chen。
文摘Resveratrol(RSV),as a functional food component extracted from natural plants,has been widely studied and recognized in preventing and treating various diseases,with major mechanisms including executing anti-inflammation and anti-oxidation functions,and improving mitochondrial quality.Chronic diseases as non-communicable diseases are mainly caused by multiple factors,such as physiological decline and dysfunction in the body,and have become a significant challenge on public health worldwide.It is worth noting that chronic diseases such as Alzheimer's disease(AD),Parkinson's disease(PD),muscle atrophy,cardiovascular disease,obesity,and cancer are accompanied by abnormal mitochondrial function.Therefore,targeted regulation of mitochondria may be a meaningful way to prevent and treat chronic diseases.Increasing evidence has confirmed that RSV is actively involved in regulating mitochondria,and it has become an essential consideration to prevent and treat chronic diseases through targeting mitochondria and improving corresponding functions.In this article,current studies on RSV to optimize mitochondrial quality for preventing and alleviating chronic disease are systematically summarized,which can provide a theoretical reference for the development of functional foods or drugs to combat chronic diseases.
基金supported by the Natural Science Foundation of Heilongjiang Province(No.LH2021H009).
文摘Objective Keshan disease(KD)is a myocardial mitochondrial disease closely related to insufficient selenium(Se)and protein intake.PTEN induced putative kinase 1(PINK1)/Parkin mediated mitochondrial autophagy regulates various physiological and pathological processes in the body.This study aimed to elucidate the relationship between PINK1/Parkin-regulated mitochondrial autophagy and KD-related myocardial injury.Methods A low Se and low protein animal model was established.One hundred Wistar rats were randomly divided into 5 groups(control group,low Se group,low protein group,low Se+low protein group,and corn from KD area group).The JC-1 method was used to detect the mitochondrial membrane potential(MMP).ELISA was used to detect serum creatine kinase MB(CK-MB),cardiac troponin I(cTnI),and mitochondrial-glutamicoxalacetic transaminase(M-GOT)levels.RT-PCR and Western blot analysis were used to detect the expression of PINK1,Parkin,sequestome 1(P62),and microtubule-associated proteins1A/1B light chain 3B(MAP1LC3B).Results The MMP was significantly decreased and the activity of CK-MB,cTnI,and M-GOT significantly increased in each experimental group(low Se group,low protein group,low Se+low protein group and corn from KD area group)compared with the control group(P<0.05 for all).The mRNA and protein expression levels of PINK1,Parkin and MAP1LC3B were profoundly increased,and those of P62 markedly decreased in the experimental groups compared with the control group(P<0.05 for all).Conclusion Low Se and low protein levels exacerbate myocardial damage in KD by affecting the PINK1/Parkin-mediated mitochondrial autophagy pathway.
