Background:Recurrent acute cholecystitis(RAC)can occur after non-surgical treatment for acute cholecystitis(AC),and can be more severe in comparison to the first episode of AC.Low skeletal muscle mass or adiposity hav...Background:Recurrent acute cholecystitis(RAC)can occur after non-surgical treatment for acute cholecystitis(AC),and can be more severe in comparison to the first episode of AC.Low skeletal muscle mass or adiposity have various effects in several diseases.We aimed to clarify the relationship between RAC and body parameters.Methods:Patients with AC who were treated at our hospital between January 2011 and March 2022 were enrolled.The psoas muscle mass and adipose tissue area at the third lumbar level were measured using computed tomography at the first episode of AC.The areas were divided by height to obtain the psoas muscle mass index(PMI)and subcutaneous/visceral adipose tissue index(SATI/VATI).According to median VATI,SATI and PMI values by sex,patients were divided into the high and low PMI groups.We performed propensity score matching to eliminate the baseline differences between the high PMI and low PMI groups and analyzed the cumulative incidence and predictors of RAC.Results:The entire cohort was divided into the high PMI(n=81)and low PMI(n=80)groups.In the propensity score-matched cohort there were 57 patients in each group.In Kaplan-Meier analysis,the low PMI group and the high VATI group had a significantly higher cumulative incidence of RAC than their counterparts(log-rank P=0.001 and 0.015,respectively).In a multivariate Cox regression analysis,the hazard ratios of low PMI and low VATI for RAC were 5.250(95%confidence interval 1.083-25.450,P=0.039)and 0.158(95%confidence interval:0.026-0.937,P=0.042),respectively.Conclusions:Low skeletal muscle mass and high visceral adiposity were independent risk factors for RAC.展开更多
Amyotrophic lateral sclerosis is a fatal multisystemic neurodegenerative disease with motor neurons being a primary target.Although progressive weakness is a hallmark feature of amyotrophic lateral sclerosis,there is ...Amyotrophic lateral sclerosis is a fatal multisystemic neurodegenerative disease with motor neurons being a primary target.Although progressive weakness is a hallmark feature of amyotrophic lateral sclerosis,there is considerable heterogeneity,including clinical presentation,progression,and the underlying triggers for disease initiation.Based on longitudinal studies with families harboring amyotrophic lateral sclerosis-associated gene mutations,it has become apparent that overt disease is preceded by a prodromal phase,possibly in years,where compensatory mechanisms delay symptom onset.Since 85-90%of amyotrophic lateral sclerosis is sporadic,there is a strong need for identifying biomarkers that can detect this prodromal phase as motor neurons have limited capacity for regeneration.Current Food and Drug Administration-approved therapies work by slowing the degenerative process and are most effective early in the disease.Skeletal muscle,including the neuromuscular junction,manifests abnormalities at the earliest stages of the disease,before motor neuron loss,making it a promising source for identifying biomarkers of the prodromal phase.The accessibility of muscle through biopsy provides a lens into the distal motor system at earlier stages and in real time.The advent of“omics”technology has led to the identification of numerous dysregulated molecules in amyotrophic lateral sclerosis muscle,ranging from coding and non-coding RNAs to proteins and metabolites.This technology has opened the door for identifying biomarkers of disease activity and providing insight into disease mechanisms.A major challenge is correlating the myriad of dysregulated molecules with clinical or histological progression and understanding their relevance to presymptomatic phases of disease.There are two major goals of this review.The first is to summarize some of the biomarkers identified in human amyotrophic lateral sclerosis muscle that have a clinicopathological correlation with disease activity,evidence of a similar dysregulation in the SOD1G93A mouse during presymptomatic stages,and evidence of progressive change during disease progression.The second goal is to review the molecular pathways these biomarkers reflect and their potential role in mitigating or promoting disease progression,and as such,their potential as therapeutic targets in amyotrophic lateral sclerosis.展开更多
Objective:To evaluate the effects of Catalpa bignonioides fruit extract on the promotion of muscle growth and muscular capacity in vitro and in vivo.Methods:Cell viability was measured using the 3-(4,5-dimethylthiazol...Objective:To evaluate the effects of Catalpa bignonioides fruit extract on the promotion of muscle growth and muscular capacity in vitro and in vivo.Methods:Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Cell proliferation was assessed using a 5-bromo-2’-deoxyuridine(BrdU)assay kit.Western blot analysis was performed to determine the protein expressions of related factors.The effects of Catalpa bignonioides extract were investigated in mice using the treadmill exhaustion test and whole-limb grip strength assay.Chemical composition analysis was performed using high-performance liquid chromatography(HPLC).Results:Catalpa bignonioides extract increased the proliferation of C2C12 mouse myoblasts by activating the Akt/mTOR signaling pathway.It also induced metabolic changes,increasing the number of mitochondria and glucose metabolism by phosphorylating adenosine monophosphate-activated protein kinase.In an in vivo study,the extract-treated mice showed improved motor abilities,such as muscular endurance and grip strength.Additionally,HPLC analysis showed that vanillic acid may be the main component of the Catalpa bignonioides extract that enhanced muscle strength.Conclusions:Catalpa bignonioides improves exercise performance through regulation of growth and metabolism in skeletal muscles,suggesting its potential as an effective natural agent for improving muscular strength.展开更多
Over the course of several decades,robust research has firmly established the significance of mitochondrial pathology as a central contributor to the onset of skeletal muscle atrophy in individuals with diabetes.Howev...Over the course of several decades,robust research has firmly established the significance of mitochondrial pathology as a central contributor to the onset of skeletal muscle atrophy in individuals with diabetes.However,the specific intricacies governing this process remain elusive.Extensive evidence highlights that individuals with diabetes regularly confront the severe consequences of skeletal muscle degradation.Deciphering the sophisticated mechanisms at the core of this pathology requires a thorough and meticulous exploration into the nuanced factors intricately associated with mitochondrial dysfunction.展开更多
Age-dependent loss of skeletal muscle mass and function is a feature of sarcopenia,and increases the risk of many aging-related metabolic diseases.Here,we report phenotypic and single-nucleus transcriptomic analyses o...Age-dependent loss of skeletal muscle mass and function is a feature of sarcopenia,and increases the risk of many aging-related metabolic diseases.Here,we report phenotypic and single-nucleus transcriptomic analyses of non-human primate skeletal muscle aging.A higher transcriptional fluctuation was observed in myonuclei relative to other interstitial cell types,indicating a higher susceptibility of skeletal muscle fiber to aging.We found a downregulation of Foxo3 in aged primate skeletal muscle,and identi-fied FOxo3 as a hub transcription factor maintaining skeletal muscle homeostasis.Through the establishment of a complementary experimental pipeline based on a human pluripotent stem cell-derived myotube model,we revealed that silence of Foxo3 accelerates human myotube senescence,whereas genetic activation of endogenous FOxO3 alleviates human myotube aging.Altogether,based on a combination of monkey skeletal muscle and human myotube aging research models,we unraveled the pivotal role of the FOxO3 in safeguarding primate skeletal muscle from aging,providing a comprehensive resource for the development of clinical diagnosis and targeted therapeutic interventions against human skeletal muscle aging and the onset of sarcopenia along with aging-relateddisorders.展开更多
Spinal cord injuries affect nearly five to ten individuals per million every year. Spinal cord injury causes damage to the nerves, muscles, and the tissue surrounding the spinal cord. Depending on the severity, spinal...Spinal cord injuries affect nearly five to ten individuals per million every year. Spinal cord injury causes damage to the nerves, muscles, and the tissue surrounding the spinal cord. Depending on the severity, spinal injuries are linked to degeneration of axons and myelin, resulting in neuronal impairment and skeletal muscle weakness and atrophy. The protection of neurons and promotion of myelin regeneration during spinal cord injury is important for recovery of function following spinal cord injury. Current treatments have little to no effect on spinal cord injury and neurogenic muscle loss. Clemastine, an Food and Drug Administration-approved antihistamine drug, reduces inflammation, protects cells, promotes remyelination, and preserves myelin integrity. Recent clinical evidence suggests that clemastine can decrease the loss of axons after spinal cord injury, stimulating the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes that are capable of myelination. While clemastine can aid not only in the remyelination and preservation of myelin sheath integrity, it also protects neurons. However, its role in neurogenic muscle loss remains unclear. This review discusses the pathophysiology of spinal cord injury, and the role of clemastine in the protection of neurons, myelin, and axons as well as attenuation of skeletal muscle loss following spinal cord injury.展开更多
Objective:The present study was conducted to demonstrate the age-dependent changes in skeletal muscle mass and visceral fat area in a population of Chinese adults aged 30-92 years old.Methods:A total of 6669 healthy C...Objective:The present study was conducted to demonstrate the age-dependent changes in skeletal muscle mass and visceral fat area in a population of Chinese adults aged 30-92 years old.Methods:A total of 6669 healthy Chinese men and 4494 healthy Chinese women aged 30-92 years old were assessed for their skeletal muscle mass and visceral fat area.Results:The results showed age-dependent decreases in the total skeletal muscle mass indexes in both men and women aged 40-92 years old as well as age-dependent increases in the visceral fat area in men aged 30-92 years old and in women aged 30-80 years old.Multivariate regression models showed that the total skeletal muscle mass index was positively associated with the body mass index and negatively associated with the age and visceral fat area in both sexes.Conclusion:The loss of skeletal muscle mass becomes obvious at approximately 50 years of age,and the visceral fat area commences to increase at approximately 40 years of age in this Chinese population.展开更多
Skeletal muscle regeneration is a complex process where various cell types and cytokines are involved.Single-cell RNA-sequencing (scRNA-seq) provides the opportunity to deconvolute heterogeneous tissue into individual...Skeletal muscle regeneration is a complex process where various cell types and cytokines are involved.Single-cell RNA-sequencing (scRNA-seq) provides the opportunity to deconvolute heterogeneous tissue into individual cells based on their transcriptomic profiles.Recent scRNA-seq studies on mouse muscle regeneration have provided insights to understand the transcriptional dynamics that underpin muscle regeneration.However,a database to investigate gene expression profiling during skeletal muscle regeneration at the single-cell level is lacking.Here,we collected over 105 000 cells at 7 key regenerative time-points and non-injured muscles and developed a database,the Singlecell Skeletal Muscle Regeneration Database (SCSMRD).SCSMRD allows users to search the dynamic expression profiles of genes of interest across different cell types during the skeletal muscle regeneration process.It also provides a network to show the activity of regulons in different cell types at different time points.Pesudotime analysis showed the state changes trajectory of muscle stem cells (MuSCs) during skeletal muscle regeneration.This database is freely available at https://scsmrd.fengs-lab.com.展开更多
Insulin resistance is a hallmark of type-2 diabetes(T2D)pathogenesis.Because skeletal muscle(SkM)is the major tissue for insulin-mediated glucose disposal,insulin resistance in SkM is considered a major risk factor fo...Insulin resistance is a hallmark of type-2 diabetes(T2D)pathogenesis.Because skeletal muscle(SkM)is the major tissue for insulin-mediated glucose disposal,insulin resistance in SkM is considered a major risk factor for developing T2D.Thus,the identifi cation of compounds that enhance the ability of SkM to take up glucose is a promising strategy for preventing T2D.Our previous work showed that kaempferol,a fl avonol present in many foods,improves insulin sensitivity in obese mice,however,the mechanism underlying this beneficial action remains unclear.Here,we show that kaempferol directly stimulates glucose uptake and prevents lipotoxicity-impaired glucose uptake in primary human SkM.Kaempferol stimulates Akt phosphorylation in a time-dependent manner in human SkM cells.The effect of kaempferol on glucose uptake was blunted by inhibition of glucose transporter 4,phosphoinositide 3-kinase(PI3K),or AMPK.In addition,kaempferol induced AMPK phosphorylation,and inhibition of AMPK prevented kaempferol-stimulated Akt phosphorylation.In vivo,kaempferol administration induced rapid glucose disposal accompanied with increased Akt and AMPK phosphorylation in SkM tissue of the mice.Taken together,these fi ndings suggest that kaempferol stimulates glucose uptake in SkM via an AMPK/Akt dependent mechanism,and it may be a viable therapeutic agent for insulin resistance.展开更多
This review highlights some established and some more contemporary mechanisms responsible for heart failure(HF)-induced skeletal muscle wasting and weakness.We first describe the effects of HF on the relationship betw...This review highlights some established and some more contemporary mechanisms responsible for heart failure(HF)-induced skeletal muscle wasting and weakness.We first describe the effects of HF on the relationship between protein synthesis and degradation rates,which determine muscle mass,the involvement of the satellite cells for continual muscle regeneration,and changes in myofiber calcium homeostasis linked to contractile dysfunction.We then highlight key mechanistic effects of both aerobic and resistance exercise training on skeletal muscle in HF and outline its application as a beneficial treatment.Overall,HF causes multiple impairments related to autophagy,anabolic-catabolic signaling,satellite cell proliferation,and calcium homeostasis,which together promote fiber atrophy,contractile dysfunction,and impaired regeneration.Although both wasting and weakness are partly rescued by aerobic and resistance exercise training in HF,the effects of satellite cell dynamics remain poorly explored.展开更多
The growth and development of skeletal muscle also determine the meat production of yak, ultimately affecting the economic benefits. Hence, improving growth performance is a top priority in the yak industry. Skeletal ...The growth and development of skeletal muscle also determine the meat production of yak, ultimately affecting the economic benefits. Hence, improving growth performance is a top priority in the yak industry. Skeletal muscle development is a complex process involving the regulation of several genes, including microRNAs(miRNAs). However,the transcription of miRNAs in yak skeletal muscle during prenatal to postnatal stages is unknown. We used small RNA sequencing(small RNA-Seq) to determine the global miRNAs of longissimus dorsi muscle from yak(the samples were collected from three fetuses and three adults). Totally 264 differently expressed miRNAs(|log2(fold change)|>1and P-value≤0.05) were detected between the two groups. Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analysis showed that differently expressed miRNAs-targeted genes participated in pathways associated with muscle development, such as MAPK, PI3K-Akt, and Hippo signaling pathways, etc. MiR-652, which was up-regulated in the fetal group, was transfected into C2C12 myoblasts to examine its role. miR-652 promoted(P≤0.05)proliferation and differentiation, but inhibited(P≤0.001) apoptosis at early period. Furthermore, miR-652 reduced(P≤0.001) the proportion of C2C12 myoblasts in the G1 phase while increasing(P≤0.01) the proportion of cells in the S and G2 phases. Dual-luciferase reporter assays indicated that ISL1 served as a target of miR-652. In general, these findings expand our understanding of yak skeletal muscle miRNAs, and suggested that miR-652 probably regulated myogenesis by regulating ISL1.展开更多
Background The skeletal muscle of pigs is vulnerable to oxidative damage,resulting in growth retardation.Selenoproteins are important components of antioxidant systems for animals,which are generally regulated by diet...Background The skeletal muscle of pigs is vulnerable to oxidative damage,resulting in growth retardation.Selenoproteins are important components of antioxidant systems for animals,which are generally regulated by dietary selenium(Se)level.Here,we developed the dietary oxidative stress(DOS)-inducing pig model to investigate the protective effects of selenoproteins on DOS-induced skeletal muscle growth retardation.Results Dietary oxidative stress caused porcine skeletal muscle oxidative damage and growth retardation,which is accompanied by mitochondrial dysfunction,endoplasmic reticulum(ER)stress,and protein and lipid metabolism disorders.Supplementation with Se(0.3,0.6 or 0.9 mg Se/kg)in form of hydroxy selenomethionine(OH-SeMet)linearly increased muscular Se deposition and exhibited protective effects via regulating the expression of selenotranscriptome and key selenoproteins,which was mainly reflected in lower ROS levels and higher antioxidant capacity in skeletal muscle,and the mitigation of mitochondrial dysfunction and ER stress.What’s more,selenoproteins inhibited DOS induced protein and lipid degradation and improved protein and lipid biosynthesis via regulating AKT/mTOR/S6K1 and AMPK/SREBP-1 signalling pathways in skeletal muscle.However,several parameters such as the activity of GSH-Px and T-SOD,the protein abundance of JNK2,CLPP,SELENOS and SELENOF did not show dose-dependent changes.Notably,several key selenoproteins such as MSRB1,SELENOW,SELENOM,SELENON and SELENOS play the unique roles during this protection.Conclusions Increased expression of selenoproteins by dietary OH-SeMet could synergistically alleviate mitochondrial dysfunction and ER stress,recover protein and lipid biosynthesis,thus alleviate skeletal muscle growth retardation.Our study provides preventive measure for OS-dependent skeletal muscle retardation in livestock husbandry.展开更多
Aging decreases muscle mass,strength,and functional capacity.High-salt stress seems to promote muscle aging and decrease lifespan.However,exercise delays muscle aging and increases longevity,and it may protect muscle ...Aging decreases muscle mass,strength,and functional capacity.High-salt stress seems to promote muscle aging and decrease lifespan.However,exercise delays muscle aging and increases longevity,and it may protect muscle from rapid aging induced by high-salt intake(HSI),but the molecular mechanisms are poorly understood.In this study,the flies were fed a high-salt diet and trained to exercise.Muscle CG2196(salt)gene and dSir2 gene were over-expressed by building mef2-gal4/UAS system.The results showed that both physical exercise and muscle dSir2 gene overexpression prevented HSI-induced and muscle salt overexpression-induced accelerated age-related decline of climbing index,climbing endurance,muscle NAD^(+)level,SOD activity level,dSir2 expression,and dFOXO expression,and they also prevented HSI-induced and muscle salt overexpression-induced accelerated age-related increase in muscle ROS level,MDA level,and salt gene expression.Physical exercise improved lifespan decrease induced by HSI and muscle salt overexpression.Therefore,current results indicated that high-salt stress accelerated muscle aging by decreasing muscular NAD^(+)/dSir2/dFOXO pathway activity and increasing oxidative stress.Physical exercise protected muscle from accelerated aging induced by high-salt stress through activating muscle NAD^(+)/dSir2/dFOXO pathway and enhancing muscle oxidation resistance.The combination of exercise and muscle dSir2 overexpression had the best protective effect on muscle aging and lifespan in flies.展开更多
Objective To distinguish the edema, injury, or rupture in the traumatic skeletal muscle fiber in vivo using diffusion tensor imaging (DTI) and tractography on magnetic resonance imaging (MRI). Methods The skeletal mus...Objective To distinguish the edema, injury, or rupture in the traumatic skeletal muscle fiber in vivo using diffusion tensor imaging (DTI) and tractography on magnetic resonance imaging (MRI). Methods The skeletal muscle trauma models were made in 4 rabbits (eight hindlimbs) by iron discus (weight 1.0 kg, diameter 6 cm) falling down vertically from 45 cm height to rabbits’ thighs. Conventional sequences and two-dimensional (2D) diffusion-weighted (DW) spin-echo (SE) echo planar imaging (EPI) sequence with fat suppression (b=600 s/mm^2) were performed on 1.5T MRI scanner. The grading of edema, injury, and fiber rupture in the damaged muscle were made according to their histopathological views, which was consistent with the images. The mean apparent diffusion coefficient (ADC) values and fractional anisotropy (FA) values were measured from the region of interests (ROIs) of all groups on 2D DW images used for tractography. Analysis of variance test was performed to analyze all data. Results ADC values of the areas in normal muscle, edema muscle, injury muscle, and ruptured muscle were (6.12±1.34)×10~ -3 , (6.38±1.30)×10~ -3 , (8.06±0.97)×10~ -3 , and (9.57±0.93)×10~ -3 mm~ 2 /s, respectively. There was significant difference among groups (P<0.001), but no difference between edema muscle and normal muscle group (P>0.05). The FA values of normal muscle, edema muscle, injury muscle, and ruptured muscle were 0.42±0.12, 0.36±0.12, 0.26±0.09, 0.12±0.08, respectively, with a significant difference among groups (P<0.001). In the edema muscle, the tracking cross-fiber could be seen but it decreased slightly. In the injury muscle, the tracking fiber decreased markedly. In the ruptured muscle, the transverse-orientation tracking fiber vanished, yet some interrupted longitudinal-orientation tracking fiber could be found. Conclusion The edema, injury, and rupture of muscle fiber in rabbit damaged skeletal muscle can be verified according to the ADC and the FA on DTI and tractography.展开更多
Apoptosis is highly considered as a possible mechanism in the aging process of skeletal muscle. Age-related apoptosis pathways in aging skeletal muscle are several, and apoptotic stimuli considered as initiators could...Apoptosis is highly considered as a possible mechanism in the aging process of skeletal muscle. Age-related apoptosis pathways in aging skeletal muscle are several, and apoptotic stimuli considered as initiators could be of various type, such as calcium, TNF-α and oxidative stress. In the last decade, scientific research has focused on some topics in order to establish an appropriate life- style improving the homeostasis of muscle tissue in aging. Physical exercise seems to improve cellular antioxidant defense especially when associated with a good quality of nutrition, thanks to some nutrients, such as carotenoids and oleic acid that have antioxidant properties. A combination of physical exercise, caloric restriction and diet seems to be best strategy to attenuate apoptotic pathways that lead to the loss of skeletal muscle in aging, with all consequence on the physical well-being of the elderly.展开更多
As a key coordinator of metabolism,AMP-activated protein kinase(AMPK)is vitally involved in skeletal muscle maintenance.AMPK exerts its cellular effects through its function as a serine/threonine protein kinase by reg...As a key coordinator of metabolism,AMP-activated protein kinase(AMPK)is vitally involved in skeletal muscle maintenance.AMPK exerts its cellular effects through its function as a serine/threonine protein kinase by regulating many downstream targets and plays important roles in the development and growth of skeletal muscle.AMPK is activated by phosphorylation and exerts its function as a kinase in many processes,including synthesis and degradation of proteins,mitochondrial biogenesis,glucose uptake,and fatty acid and cholesterol metabolism.Skeletal muscle atrophy is a result of various diseases or disorders and is characterized by a decrease in muscle mass.The pathogenesis and therapeutic strategies of skeletal muscle atrophy are still under investigation.In this review,we discuss the role of AMPK in skeletal muscle metabolism and atrophy.We also discuss targeting AMPK for skeletal muscle treatment,including exercise,AMPK activators including 5-amino-4-imidazolecarboxamide ribonucleoside and metformin,and low-level lasers.These studies show the important roles of AMPK in regulating muscle metabolism and function;thus,the treatment of skeletal muscle atrophy needs to take into account the roles of AMPK.展开更多
[Objectives]This study was conducted to investigate the effects of Astragalus membranaceus in different groups on energy metabolism and CNTF protein expression in skeletal muscle of exercise-induced fatigue rats.[Meth...[Objectives]This study was conducted to investigate the effects of Astragalus membranaceus in different groups on energy metabolism and CNTF protein expression in skeletal muscle of exercise-induced fatigue rats.[Methods]Thirty-five clean male SD rats were randomly divided into a normal group,and low-,meddle-and high-dose groups of A.membranaceus aqueous solution,with 7 rats in each group.The low-dose,medium-dose and high-dose groups were given by gavage at 0.65,1.3 and 2.6 g/kg,respectively,while the normal group and the model group were given normal food and water.The weight of rats was observed.The contents of serum urea,lactate,muscle glycogen,liver glycogen and CNTF expression were detected.[Results]After modeling,compared with the normal group,the serum lactate and urea contents of rats in the model group significantly increased(P<0.01),while the muscle glycogen content(P<0.01)and liver glycogen content(P<0.05)of the skeletal muscle significantly decreased.Compared with the model group,the low-,meddle-and high-dose groups of A.membranaceus significantly reduced the levels of lactate and urea in serum(P<0.01),while the levels of muscle glycogen and liver glycogen in the skeletal muscle significantly increased(P<0.01,P<0.05).[Conclusions]This study provides a good research foundation for the treatment of exercise-induced fatigue using traditional Chinese herb A.membranaceus in modern clinical practice.展开更多
Coordinated contraction of skeletal muscles relies on selective connections between the muscles and multiple classes of the spinal motoneuro ns.Howeve r,current research on the spatial location of the spinal motoneuro...Coordinated contraction of skeletal muscles relies on selective connections between the muscles and multiple classes of the spinal motoneuro ns.Howeve r,current research on the spatial location of the spinal motoneurons innervating differe nt muscles is limited.In this study,we investigated the spatial distribution and relative position of different motoneurons that control the deep muscles of the mouse hindlimbs,which were innervated by the obturator nerve,femoral nerve,inferior gluteal nerve,deep pe roneal nerve,and tibial nerve.Locations were visualized by combining a multiplex retrograde tracking technique compatible with three-dimensional imaging of solvent-cleared o rgans(3DISCO)and 3-D imaging technology based on lightsheet fluorescence microscopy(LSFM).Additionally,we propose the hypothesis that"messenger zones"exist as interlaced areas between the motoneuron pools that dominate the synergistic or antagonist muscle groups.We hypothesize that these interlaced neurons may participate in muscle coordination as messenger neurons.Analysis revealed the precise mutual positional relationships among the many motoneurons that innervate different deep muscles of the mouse.Not only do these findings update and supplement our knowledge regarding the overall spatial layout of spinal motoneurons that control mouse limb muscles,but they also provide insights into the mechanisms through which muscle activity is coordinated and the architecture of motor circuits.展开更多
Sarcopenia,or muscle loss,has been one of the hot topics in the medical field in recent years.Due to limited attention and effective treatments for sarcopenia in the past,many patients,especially the elderly,suffered ...Sarcopenia,or muscle loss,has been one of the hot topics in the medical field in recent years.Due to limited attention and effective treatments for sarcopenia in the past,many patients,especially the elderly,suffered irreversible damage to their motor function caused by sarcopenia.However,recent scientific studies have found that the occurrence and development of sarcopenia are closely related to the function and quantity of muscle satellite cells.This article briefly discusses the relationship between muscle satellite cells and sarcopenia.展开更多
We aimed to investigate the association between mobility and skeletal muscle strength by using magnetic resonance diffusion tensor imaging (DTI). This study included 20 healthy male volunteers (mean age, 21.8 ± 1...We aimed to investigate the association between mobility and skeletal muscle strength by using magnetic resonance diffusion tensor imaging (DTI). This study included 20 healthy male volunteers (mean age, 21.8 ± 1.1 years). The maximum voluntary strength (MVC) of each participant was measured with the ankle joint in plantar and dorsal flexion using an instrument for measuring muscle strength. Moreover, magnetic resonance imaging (MRI) was performed with the ankle joint at rest, in plantar flexion, and in dorsal flexion. For imaging, a 1.5-T MRI device was used, and a diffusion-weighted stimulated echo-planar imaging pulse sequence. Tensor eigenvalues (λ), fractional anisotropy (FA), and the apparent diffusion coefficient (ADC) were calculated from data obtained by DTI. The resulting MRI data were compared to the data on muscle mobility or strength and statistically analyzed. Regarding changes in DTI indices during muscle movements, anisotropy of the tibialis anterior was significantly increased from rest to plantar flexion (P < 0.01), whereas no significant change was observed in dorsal flexion (n.s.). In contrast, the extent of significant changes in anisotropy of the medial gastrocnemius (mGC) and soleus (SOL) was small at plantar flexion (mGC, P < 0.01;SOL, n.s.), whereas the indices were significantly increased at dorsal flexion (P < 0.01). Regarding the correlation between MVC of each skeletal muscle and the DTI indices, FA and λ3 were significantly correlated in movements involving the muscles, whereas no significant correlation was observed in movements not involving them. Changes in intramuscular water molecules by elongation and contraction of the skeletal muscle fibers could be assumed to affect changes in diffusional anisotropy. When muscles contract, the space between myocytes was reduced and they might become increasingly dense. Moreover, diffusional anisotropy increased with increasing MVC, whereas ADC remained unchanged. DTI was suggested to produce measurements similar to the degree of muscle strength.展开更多
基金This study was approved by the Ethics Committee of Kyushu Rosai Hospital Moji Medical Center(No:04-01,date of approval:June 2,2022).This study was conducted in compliance with the principles of the Declaration of Helsinki.
文摘Background:Recurrent acute cholecystitis(RAC)can occur after non-surgical treatment for acute cholecystitis(AC),and can be more severe in comparison to the first episode of AC.Low skeletal muscle mass or adiposity have various effects in several diseases.We aimed to clarify the relationship between RAC and body parameters.Methods:Patients with AC who were treated at our hospital between January 2011 and March 2022 were enrolled.The psoas muscle mass and adipose tissue area at the third lumbar level were measured using computed tomography at the first episode of AC.The areas were divided by height to obtain the psoas muscle mass index(PMI)and subcutaneous/visceral adipose tissue index(SATI/VATI).According to median VATI,SATI and PMI values by sex,patients were divided into the high and low PMI groups.We performed propensity score matching to eliminate the baseline differences between the high PMI and low PMI groups and analyzed the cumulative incidence and predictors of RAC.Results:The entire cohort was divided into the high PMI(n=81)and low PMI(n=80)groups.In the propensity score-matched cohort there were 57 patients in each group.In Kaplan-Meier analysis,the low PMI group and the high VATI group had a significantly higher cumulative incidence of RAC than their counterparts(log-rank P=0.001 and 0.015,respectively).In a multivariate Cox regression analysis,the hazard ratios of low PMI and low VATI for RAC were 5.250(95%confidence interval 1.083-25.450,P=0.039)and 0.158(95%confidence interval:0.026-0.937,P=0.042),respectively.Conclusions:Low skeletal muscle mass and high visceral adiposity were independent risk factors for RAC.
基金supported by NIH Grants R01NS092651 and R21NS111275-01the Department of Veterans Affairs,BX001148 and BX005899(to PHK)。
文摘Amyotrophic lateral sclerosis is a fatal multisystemic neurodegenerative disease with motor neurons being a primary target.Although progressive weakness is a hallmark feature of amyotrophic lateral sclerosis,there is considerable heterogeneity,including clinical presentation,progression,and the underlying triggers for disease initiation.Based on longitudinal studies with families harboring amyotrophic lateral sclerosis-associated gene mutations,it has become apparent that overt disease is preceded by a prodromal phase,possibly in years,where compensatory mechanisms delay symptom onset.Since 85-90%of amyotrophic lateral sclerosis is sporadic,there is a strong need for identifying biomarkers that can detect this prodromal phase as motor neurons have limited capacity for regeneration.Current Food and Drug Administration-approved therapies work by slowing the degenerative process and are most effective early in the disease.Skeletal muscle,including the neuromuscular junction,manifests abnormalities at the earliest stages of the disease,before motor neuron loss,making it a promising source for identifying biomarkers of the prodromal phase.The accessibility of muscle through biopsy provides a lens into the distal motor system at earlier stages and in real time.The advent of“omics”technology has led to the identification of numerous dysregulated molecules in amyotrophic lateral sclerosis muscle,ranging from coding and non-coding RNAs to proteins and metabolites.This technology has opened the door for identifying biomarkers of disease activity and providing insight into disease mechanisms.A major challenge is correlating the myriad of dysregulated molecules with clinical or histological progression and understanding their relevance to presymptomatic phases of disease.There are two major goals of this review.The first is to summarize some of the biomarkers identified in human amyotrophic lateral sclerosis muscle that have a clinicopathological correlation with disease activity,evidence of a similar dysregulation in the SOD1G93A mouse during presymptomatic stages,and evidence of progressive change during disease progression.The second goal is to review the molecular pathways these biomarkers reflect and their potential role in mitigating or promoting disease progression,and as such,their potential as therapeutic targets in amyotrophic lateral sclerosis.
基金supported by Korea Environment Industry&Technology Institute through Project to make multi-ministerial national biological research resources more advanced Project,funded by Korea Ministry of Environment(grant number RS-2023-00230403).
文摘Objective:To evaluate the effects of Catalpa bignonioides fruit extract on the promotion of muscle growth and muscular capacity in vitro and in vivo.Methods:Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Cell proliferation was assessed using a 5-bromo-2’-deoxyuridine(BrdU)assay kit.Western blot analysis was performed to determine the protein expressions of related factors.The effects of Catalpa bignonioides extract were investigated in mice using the treadmill exhaustion test and whole-limb grip strength assay.Chemical composition analysis was performed using high-performance liquid chromatography(HPLC).Results:Catalpa bignonioides extract increased the proliferation of C2C12 mouse myoblasts by activating the Akt/mTOR signaling pathway.It also induced metabolic changes,increasing the number of mitochondria and glucose metabolism by phosphorylating adenosine monophosphate-activated protein kinase.In an in vivo study,the extract-treated mice showed improved motor abilities,such as muscular endurance and grip strength.Additionally,HPLC analysis showed that vanillic acid may be the main component of the Catalpa bignonioides extract that enhanced muscle strength.Conclusions:Catalpa bignonioides improves exercise performance through regulation of growth and metabolism in skeletal muscles,suggesting its potential as an effective natural agent for improving muscular strength.
基金the Foundation of State Key Laboratory of Component-based Chinese Medicine,No.CBCM2023107National Natural Science Foundation of China,No.81901853Specially Funded Scientific Research Project of the Fourth Affiliated Hospital of Harbin Medical University,No.HYDSYTB202126.
文摘Over the course of several decades,robust research has firmly established the significance of mitochondrial pathology as a central contributor to the onset of skeletal muscle atrophy in individuals with diabetes.However,the specific intricacies governing this process remain elusive.Extensive evidence highlights that individuals with diabetes regularly confront the severe consequences of skeletal muscle degradation.Deciphering the sophisticated mechanisms at the core of this pathology requires a thorough and meticulous exploration into the nuanced factors intricately associated with mitochondrial dysfunction.
基金supported by the Strategic Priority Research Program of the Chinese Academy of Sciences(No.XDA16000000)the National Natural Science Foundation of China(Nos.82071588,81921006,82125011,92149301,92168201,92049116,32121001,82192863,91949209,92049304,82122024,82001477,31900523,81861168034,32000500,82271600,82201714)+10 种基金the National Key Research and Development Program of China(Nos.2018YFC2000100,2020YFA0804000,2018YFA0107203,2020YFA0112200,2021YFF1201005,2021ZD0202401,2018YFC2000400,2020YFA0113400,2021YFE0111800,2022YFA1103700)the Program of the Beijing Natural Science Foundation(No.Z190019)K.C.Wong Education Foundation(Nos.GJTD-2019-06,GJTD-2019-08)Beijing Medical Research(2021-8)the Pilot Project for Public Welfare Development and Reform of Beijing-affliated Medical Research Institutes(No.11000022T000000461062)Young Elite Scientists Sponsorship Program by CAST(Nos.YESS20200012,YESS20210002)CAS Project for Young Scientists in Basic Research(No.YSBR-076,YSBR-012,YSBR-036)Youth Innovation Promotion Association of CAS(Nos.E1CAZW0401,2020085,2022083)the Informatization Plan of Chinese Academy of Sciences(Nos.CAS-WX2022SDC-XK14,CASWX2021SF-0301,CAS-WX2021SF-0101)the Tencent Foundation(No.2021-1045),CAMS Innovation Fund for Medical Sciences(No.2021-12M-1-050)the Fellowship of China Postdoctoral Science Foundation(2022M712216).
文摘Age-dependent loss of skeletal muscle mass and function is a feature of sarcopenia,and increases the risk of many aging-related metabolic diseases.Here,we report phenotypic and single-nucleus transcriptomic analyses of non-human primate skeletal muscle aging.A higher transcriptional fluctuation was observed in myonuclei relative to other interstitial cell types,indicating a higher susceptibility of skeletal muscle fiber to aging.We found a downregulation of Foxo3 in aged primate skeletal muscle,and identi-fied FOxo3 as a hub transcription factor maintaining skeletal muscle homeostasis.Through the establishment of a complementary experimental pipeline based on a human pluripotent stem cell-derived myotube model,we revealed that silence of Foxo3 accelerates human myotube senescence,whereas genetic activation of endogenous FOxO3 alleviates human myotube aging.Altogether,based on a combination of monkey skeletal muscle and human myotube aging research models,we unraveled the pivotal role of the FOxO3 in safeguarding primate skeletal muscle from aging,providing a comprehensive resource for the development of clinical diagnosis and targeted therapeutic interventions against human skeletal muscle aging and the onset of sarcopenia along with aging-relateddisorders.
基金supported in part by funding from the Veterans Administration (1IOBX001262, 1I01 BX004269)South Carolina State Spinal Cord Injury Research Fund (SCIRF-2015P-01, SCIRF-2015P-04, SCIRF-2015-I-01, SCIRF#2016 I-03, and SCIRF#2018 I-01)(to AH)+1 种基金supported in part by funding from the National Institutes of Health (1R21NS118393-01)(to AH)a Research Career Scientist award (#IK6BX005964) from the Department of veterans Affairs。
文摘Spinal cord injuries affect nearly five to ten individuals per million every year. Spinal cord injury causes damage to the nerves, muscles, and the tissue surrounding the spinal cord. Depending on the severity, spinal injuries are linked to degeneration of axons and myelin, resulting in neuronal impairment and skeletal muscle weakness and atrophy. The protection of neurons and promotion of myelin regeneration during spinal cord injury is important for recovery of function following spinal cord injury. Current treatments have little to no effect on spinal cord injury and neurogenic muscle loss. Clemastine, an Food and Drug Administration-approved antihistamine drug, reduces inflammation, protects cells, promotes remyelination, and preserves myelin integrity. Recent clinical evidence suggests that clemastine can decrease the loss of axons after spinal cord injury, stimulating the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes that are capable of myelination. While clemastine can aid not only in the remyelination and preservation of myelin sheath integrity, it also protects neurons. However, its role in neurogenic muscle loss remains unclear. This review discusses the pathophysiology of spinal cord injury, and the role of clemastine in the protection of neurons, myelin, and axons as well as attenuation of skeletal muscle loss following spinal cord injury.
基金supported by the Basic Public Welfare Research Program of Zhejiang Province(No.LGF20H020009)a Taizhou Science and Technology Plan Project(No.22ywb105)。
文摘Objective:The present study was conducted to demonstrate the age-dependent changes in skeletal muscle mass and visceral fat area in a population of Chinese adults aged 30-92 years old.Methods:A total of 6669 healthy Chinese men and 4494 healthy Chinese women aged 30-92 years old were assessed for their skeletal muscle mass and visceral fat area.Results:The results showed age-dependent decreases in the total skeletal muscle mass indexes in both men and women aged 40-92 years old as well as age-dependent increases in the visceral fat area in men aged 30-92 years old and in women aged 30-80 years old.Multivariate regression models showed that the total skeletal muscle mass index was positively associated with the body mass index and negatively associated with the age and visceral fat area in both sexes.Conclusion:The loss of skeletal muscle mass becomes obvious at approximately 50 years of age,and the visceral fat area commences to increase at approximately 40 years of age in this Chinese population.
基金supported by the National Natural Science Foundation of China(31972539 and 32102513)the Science,Technology,and Innovation Commission of Shenzhen Municipality,China(JCYJ20180306173644635)+2 种基金the Fundamental Research Funds for the Central Universities,China(G2020KY05109)the Natural Science Basic Research Program of Shaanxi Province,China(2022JQ-644)the Basic Research Programs of Taicang,China(TC2021JC14)。
文摘Skeletal muscle regeneration is a complex process where various cell types and cytokines are involved.Single-cell RNA-sequencing (scRNA-seq) provides the opportunity to deconvolute heterogeneous tissue into individual cells based on their transcriptomic profiles.Recent scRNA-seq studies on mouse muscle regeneration have provided insights to understand the transcriptional dynamics that underpin muscle regeneration.However,a database to investigate gene expression profiling during skeletal muscle regeneration at the single-cell level is lacking.Here,we collected over 105 000 cells at 7 key regenerative time-points and non-injured muscles and developed a database,the Singlecell Skeletal Muscle Regeneration Database (SCSMRD).SCSMRD allows users to search the dynamic expression profiles of genes of interest across different cell types during the skeletal muscle regeneration process.It also provides a network to show the activity of regulons in different cell types at different time points.Pesudotime analysis showed the state changes trajectory of muscle stem cells (MuSCs) during skeletal muscle regeneration.This database is freely available at https://scsmrd.fengs-lab.com.
基金partially supported by grants from Diabetes Action Research and Education Foundation。
文摘Insulin resistance is a hallmark of type-2 diabetes(T2D)pathogenesis.Because skeletal muscle(SkM)is the major tissue for insulin-mediated glucose disposal,insulin resistance in SkM is considered a major risk factor for developing T2D.Thus,the identifi cation of compounds that enhance the ability of SkM to take up glucose is a promising strategy for preventing T2D.Our previous work showed that kaempferol,a fl avonol present in many foods,improves insulin sensitivity in obese mice,however,the mechanism underlying this beneficial action remains unclear.Here,we show that kaempferol directly stimulates glucose uptake and prevents lipotoxicity-impaired glucose uptake in primary human SkM.Kaempferol stimulates Akt phosphorylation in a time-dependent manner in human SkM cells.The effect of kaempferol on glucose uptake was blunted by inhibition of glucose transporter 4,phosphoinositide 3-kinase(PI3K),or AMPK.In addition,kaempferol induced AMPK phosphorylation,and inhibition of AMPK prevented kaempferol-stimulated Akt phosphorylation.In vivo,kaempferol administration induced rapid glucose disposal accompanied with increased Akt and AMPK phosphorylation in SkM tissue of the mice.Taken together,these fi ndings suggest that kaempferol stimulates glucose uptake in SkM via an AMPK/Akt dependent mechanism,and it may be a viable therapeutic agent for insulin resistance.
基金supported by Heart Research UK(Grant number 119191)British Heart Foundation(Grant number 124055)。
文摘This review highlights some established and some more contemporary mechanisms responsible for heart failure(HF)-induced skeletal muscle wasting and weakness.We first describe the effects of HF on the relationship between protein synthesis and degradation rates,which determine muscle mass,the involvement of the satellite cells for continual muscle regeneration,and changes in myofiber calcium homeostasis linked to contractile dysfunction.We then highlight key mechanistic effects of both aerobic and resistance exercise training on skeletal muscle in HF and outline its application as a beneficial treatment.Overall,HF causes multiple impairments related to autophagy,anabolic-catabolic signaling,satellite cell proliferation,and calcium homeostasis,which together promote fiber atrophy,contractile dysfunction,and impaired regeneration.Although both wasting and weakness are partly rescued by aerobic and resistance exercise training in HF,the effects of satellite cell dynamics remain poorly explored.
基金supported by the Agricultural Science and Technology Innovation Program, CAAS (25-LZIHPS-01)the China Agriculture Research System of MOF and MARA (CARS-37)the National Natural Science Foundation of China (32102500)。
文摘The growth and development of skeletal muscle also determine the meat production of yak, ultimately affecting the economic benefits. Hence, improving growth performance is a top priority in the yak industry. Skeletal muscle development is a complex process involving the regulation of several genes, including microRNAs(miRNAs). However,the transcription of miRNAs in yak skeletal muscle during prenatal to postnatal stages is unknown. We used small RNA sequencing(small RNA-Seq) to determine the global miRNAs of longissimus dorsi muscle from yak(the samples were collected from three fetuses and three adults). Totally 264 differently expressed miRNAs(|log2(fold change)|>1and P-value≤0.05) were detected between the two groups. Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analysis showed that differently expressed miRNAs-targeted genes participated in pathways associated with muscle development, such as MAPK, PI3K-Akt, and Hippo signaling pathways, etc. MiR-652, which was up-regulated in the fetal group, was transfected into C2C12 myoblasts to examine its role. miR-652 promoted(P≤0.05)proliferation and differentiation, but inhibited(P≤0.001) apoptosis at early period. Furthermore, miR-652 reduced(P≤0.001) the proportion of C2C12 myoblasts in the G1 phase while increasing(P≤0.01) the proportion of cells in the S and G2 phases. Dual-luciferase reporter assays indicated that ISL1 served as a target of miR-652. In general, these findings expand our understanding of yak skeletal muscle miRNAs, and suggested that miR-652 probably regulated myogenesis by regulating ISL1.
基金supported by the National Natural Science Foundation of China(No.31772643 and 31272468)the Special Research Funding for Discipline Construction in Sichuan Agricultural University(No.03570126)Adisseo France(18SES533).
文摘Background The skeletal muscle of pigs is vulnerable to oxidative damage,resulting in growth retardation.Selenoproteins are important components of antioxidant systems for animals,which are generally regulated by dietary selenium(Se)level.Here,we developed the dietary oxidative stress(DOS)-inducing pig model to investigate the protective effects of selenoproteins on DOS-induced skeletal muscle growth retardation.Results Dietary oxidative stress caused porcine skeletal muscle oxidative damage and growth retardation,which is accompanied by mitochondrial dysfunction,endoplasmic reticulum(ER)stress,and protein and lipid metabolism disorders.Supplementation with Se(0.3,0.6 or 0.9 mg Se/kg)in form of hydroxy selenomethionine(OH-SeMet)linearly increased muscular Se deposition and exhibited protective effects via regulating the expression of selenotranscriptome and key selenoproteins,which was mainly reflected in lower ROS levels and higher antioxidant capacity in skeletal muscle,and the mitigation of mitochondrial dysfunction and ER stress.What’s more,selenoproteins inhibited DOS induced protein and lipid degradation and improved protein and lipid biosynthesis via regulating AKT/mTOR/S6K1 and AMPK/SREBP-1 signalling pathways in skeletal muscle.However,several parameters such as the activity of GSH-Px and T-SOD,the protein abundance of JNK2,CLPP,SELENOS and SELENOF did not show dose-dependent changes.Notably,several key selenoproteins such as MSRB1,SELENOW,SELENOM,SELENON and SELENOS play the unique roles during this protection.Conclusions Increased expression of selenoproteins by dietary OH-SeMet could synergistically alleviate mitochondrial dysfunction and ER stress,recover protein and lipid biosynthesis,thus alleviate skeletal muscle growth retardation.Our study provides preventive measure for OS-dependent skeletal muscle retardation in livestock husbandry.
基金This work is supported by the National Natural Science Foundation of China(NSFC)(32000832)Province Natural Science Foundation of Shandong(ZR2020QC096).
文摘Aging decreases muscle mass,strength,and functional capacity.High-salt stress seems to promote muscle aging and decrease lifespan.However,exercise delays muscle aging and increases longevity,and it may protect muscle from rapid aging induced by high-salt intake(HSI),but the molecular mechanisms are poorly understood.In this study,the flies were fed a high-salt diet and trained to exercise.Muscle CG2196(salt)gene and dSir2 gene were over-expressed by building mef2-gal4/UAS system.The results showed that both physical exercise and muscle dSir2 gene overexpression prevented HSI-induced and muscle salt overexpression-induced accelerated age-related decline of climbing index,climbing endurance,muscle NAD^(+)level,SOD activity level,dSir2 expression,and dFOXO expression,and they also prevented HSI-induced and muscle salt overexpression-induced accelerated age-related increase in muscle ROS level,MDA level,and salt gene expression.Physical exercise improved lifespan decrease induced by HSI and muscle salt overexpression.Therefore,current results indicated that high-salt stress accelerated muscle aging by decreasing muscular NAD^(+)/dSir2/dFOXO pathway activity and increasing oxidative stress.Physical exercise protected muscle from accelerated aging induced by high-salt stress through activating muscle NAD^(+)/dSir2/dFOXO pathway and enhancing muscle oxidation resistance.The combination of exercise and muscle dSir2 overexpression had the best protective effect on muscle aging and lifespan in flies.
文摘Objective To distinguish the edema, injury, or rupture in the traumatic skeletal muscle fiber in vivo using diffusion tensor imaging (DTI) and tractography on magnetic resonance imaging (MRI). Methods The skeletal muscle trauma models were made in 4 rabbits (eight hindlimbs) by iron discus (weight 1.0 kg, diameter 6 cm) falling down vertically from 45 cm height to rabbits’ thighs. Conventional sequences and two-dimensional (2D) diffusion-weighted (DW) spin-echo (SE) echo planar imaging (EPI) sequence with fat suppression (b=600 s/mm^2) were performed on 1.5T MRI scanner. The grading of edema, injury, and fiber rupture in the damaged muscle were made according to their histopathological views, which was consistent with the images. The mean apparent diffusion coefficient (ADC) values and fractional anisotropy (FA) values were measured from the region of interests (ROIs) of all groups on 2D DW images used for tractography. Analysis of variance test was performed to analyze all data. Results ADC values of the areas in normal muscle, edema muscle, injury muscle, and ruptured muscle were (6.12±1.34)×10~ -3 , (6.38±1.30)×10~ -3 , (8.06±0.97)×10~ -3 , and (9.57±0.93)×10~ -3 mm~ 2 /s, respectively. There was significant difference among groups (P<0.001), but no difference between edema muscle and normal muscle group (P>0.05). The FA values of normal muscle, edema muscle, injury muscle, and ruptured muscle were 0.42±0.12, 0.36±0.12, 0.26±0.09, 0.12±0.08, respectively, with a significant difference among groups (P<0.001). In the edema muscle, the tracking cross-fiber could be seen but it decreased slightly. In the injury muscle, the tracking fiber decreased markedly. In the ruptured muscle, the transverse-orientation tracking fiber vanished, yet some interrupted longitudinal-orientation tracking fiber could be found. Conclusion The edema, injury, and rupture of muscle fiber in rabbit damaged skeletal muscle can be verified according to the ADC and the FA on DTI and tractography.
文摘Apoptosis is highly considered as a possible mechanism in the aging process of skeletal muscle. Age-related apoptosis pathways in aging skeletal muscle are several, and apoptotic stimuli considered as initiators could be of various type, such as calcium, TNF-α and oxidative stress. In the last decade, scientific research has focused on some topics in order to establish an appropriate life- style improving the homeostasis of muscle tissue in aging. Physical exercise seems to improve cellular antioxidant defense especially when associated with a good quality of nutrition, thanks to some nutrients, such as carotenoids and oleic acid that have antioxidant properties. A combination of physical exercise, caloric restriction and diet seems to be best strategy to attenuate apoptotic pathways that lead to the loss of skeletal muscle in aging, with all consequence on the physical well-being of the elderly.
基金supported by the Natural Science Foundation of China(Grant No.32071517,82072106)the Natural Science Basic Research Plan in Shaanxi Province of China(Grant No.2020JM-100).
文摘As a key coordinator of metabolism,AMP-activated protein kinase(AMPK)is vitally involved in skeletal muscle maintenance.AMPK exerts its cellular effects through its function as a serine/threonine protein kinase by regulating many downstream targets and plays important roles in the development and growth of skeletal muscle.AMPK is activated by phosphorylation and exerts its function as a kinase in many processes,including synthesis and degradation of proteins,mitochondrial biogenesis,glucose uptake,and fatty acid and cholesterol metabolism.Skeletal muscle atrophy is a result of various diseases or disorders and is characterized by a decrease in muscle mass.The pathogenesis and therapeutic strategies of skeletal muscle atrophy are still under investigation.In this review,we discuss the role of AMPK in skeletal muscle metabolism and atrophy.We also discuss targeting AMPK for skeletal muscle treatment,including exercise,AMPK activators including 5-amino-4-imidazolecarboxamide ribonucleoside and metformin,and low-level lasers.These studies show the important roles of AMPK in regulating muscle metabolism and function;thus,the treatment of skeletal muscle atrophy needs to take into account the roles of AMPK.
基金Supported by Undergraduate Innovation and Entrepreneurship Training Program of Guizhou University of Traditional Chinese Medicine(GZYDCHZ[2019]42)National Key R&D Plan(2019YFC1712500)Guizhou Provincial Science and Technology Planning Project(QKHHBZ[2020]3003).
文摘[Objectives]This study was conducted to investigate the effects of Astragalus membranaceus in different groups on energy metabolism and CNTF protein expression in skeletal muscle of exercise-induced fatigue rats.[Methods]Thirty-five clean male SD rats were randomly divided into a normal group,and low-,meddle-and high-dose groups of A.membranaceus aqueous solution,with 7 rats in each group.The low-dose,medium-dose and high-dose groups were given by gavage at 0.65,1.3 and 2.6 g/kg,respectively,while the normal group and the model group were given normal food and water.The weight of rats was observed.The contents of serum urea,lactate,muscle glycogen,liver glycogen and CNTF expression were detected.[Results]After modeling,compared with the normal group,the serum lactate and urea contents of rats in the model group significantly increased(P<0.01),while the muscle glycogen content(P<0.01)and liver glycogen content(P<0.05)of the skeletal muscle significantly decreased.Compared with the model group,the low-,meddle-and high-dose groups of A.membranaceus significantly reduced the levels of lactate and urea in serum(P<0.01),while the levels of muscle glycogen and liver glycogen in the skeletal muscle significantly increased(P<0.01,P<0.05).[Conclusions]This study provides a good research foundation for the treatment of exercise-induced fatigue using traditional Chinese herb A.membranaceus in modern clinical practice.
基金supported by the Chinese National General Program of the National Natural Science Foundation of China,No.82072162(to XY)。
文摘Coordinated contraction of skeletal muscles relies on selective connections between the muscles and multiple classes of the spinal motoneuro ns.Howeve r,current research on the spatial location of the spinal motoneurons innervating differe nt muscles is limited.In this study,we investigated the spatial distribution and relative position of different motoneurons that control the deep muscles of the mouse hindlimbs,which were innervated by the obturator nerve,femoral nerve,inferior gluteal nerve,deep pe roneal nerve,and tibial nerve.Locations were visualized by combining a multiplex retrograde tracking technique compatible with three-dimensional imaging of solvent-cleared o rgans(3DISCO)and 3-D imaging technology based on lightsheet fluorescence microscopy(LSFM).Additionally,we propose the hypothesis that"messenger zones"exist as interlaced areas between the motoneuron pools that dominate the synergistic or antagonist muscle groups.We hypothesize that these interlaced neurons may participate in muscle coordination as messenger neurons.Analysis revealed the precise mutual positional relationships among the many motoneurons that innervate different deep muscles of the mouse.Not only do these findings update and supplement our knowledge regarding the overall spatial layout of spinal motoneurons that control mouse limb muscles,but they also provide insights into the mechanisms through which muscle activity is coordinated and the architecture of motor circuits.
文摘Sarcopenia,or muscle loss,has been one of the hot topics in the medical field in recent years.Due to limited attention and effective treatments for sarcopenia in the past,many patients,especially the elderly,suffered irreversible damage to their motor function caused by sarcopenia.However,recent scientific studies have found that the occurrence and development of sarcopenia are closely related to the function and quantity of muscle satellite cells.This article briefly discusses the relationship between muscle satellite cells and sarcopenia.
文摘We aimed to investigate the association between mobility and skeletal muscle strength by using magnetic resonance diffusion tensor imaging (DTI). This study included 20 healthy male volunteers (mean age, 21.8 ± 1.1 years). The maximum voluntary strength (MVC) of each participant was measured with the ankle joint in plantar and dorsal flexion using an instrument for measuring muscle strength. Moreover, magnetic resonance imaging (MRI) was performed with the ankle joint at rest, in plantar flexion, and in dorsal flexion. For imaging, a 1.5-T MRI device was used, and a diffusion-weighted stimulated echo-planar imaging pulse sequence. Tensor eigenvalues (λ), fractional anisotropy (FA), and the apparent diffusion coefficient (ADC) were calculated from data obtained by DTI. The resulting MRI data were compared to the data on muscle mobility or strength and statistically analyzed. Regarding changes in DTI indices during muscle movements, anisotropy of the tibialis anterior was significantly increased from rest to plantar flexion (P < 0.01), whereas no significant change was observed in dorsal flexion (n.s.). In contrast, the extent of significant changes in anisotropy of the medial gastrocnemius (mGC) and soleus (SOL) was small at plantar flexion (mGC, P < 0.01;SOL, n.s.), whereas the indices were significantly increased at dorsal flexion (P < 0.01). Regarding the correlation between MVC of each skeletal muscle and the DTI indices, FA and λ3 were significantly correlated in movements involving the muscles, whereas no significant correlation was observed in movements not involving them. Changes in intramuscular water molecules by elongation and contraction of the skeletal muscle fibers could be assumed to affect changes in diffusional anisotropy. When muscles contract, the space between myocytes was reduced and they might become increasingly dense. Moreover, diffusional anisotropy increased with increasing MVC, whereas ADC remained unchanged. DTI was suggested to produce measurements similar to the degree of muscle strength.
