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IgA肾病患者IgA1糖基化异常及其致病机制 被引量:2

The pathopoiesis mechanism of abnormal IgA1 glycosylation in Ig A nephropathy patients
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摘要 IgA肾病(IgAN)是导致终末期肾病最常见的原发性肾小球疾病。其病理特点为IgA1在肾小球系膜区沉积,IgA1分子的异常糖基化是导致IgAN发病的关键因素。多种与IgAN相关的基因位点已经被发现。这些基因编码的细胞因子参与了IgA1糖基化异常的发病机制。此外糖基化酶缺乏、分子伴侣甲基化异常都可能导致IgA1异常糖基化。异常糖基化的IgA1可通过自我聚集或形成免疫复合物沉积于系膜区,进而刺激系膜细胞增殖、分泌系膜基质、细胞因子、趋化因子、生长因子等,导致肾小球损伤。对IgA1异常糖基化的深入研究有助于了解IgA肾病的发病机制并提供新的诊断与治疗措施。 IgA nephropathy (IgAN)is the most common primary glomerular disease that can result in end-stage renal disease,and is histologically characterized by the deposition of IgA1 in the glomerular mesangium.The abnormal IgA1 glycosylation is the key factor in the pathogenesis of IgAN.Multiple genetic loci associated with IgAN have been identified,and the cytokines coded by them are involved in the pathopoiesis mechanism of abnormal IgA1 glycosylation.In addition,the lack of glycosylase and abnormal methylation of molecular chaperone may also be involved in the aberrant glycosylation of IgA1.Abnormally glycosylated IgA1 can deposit in the mesangium through their own assembly together or formation of immunocomplex,which can subsequently stimulate mesangial cell proliferation and secretion of extracellular matrix,cytokines,chemokines,and growth factors,etc,leading to glomerular injury.In-depth research on IgA1 abnormal glycosylation will help to understand the pathogenesis of IgAN and provide new diagnosis and treatment methods.
作者 林淑芃
出处 《中华肾病研究电子杂志》 2015年第6期40-44,共5页 Chinese Journal of Kidney Disease Investigation(Electronic Edition)
基金 国家自然科学基金(31200589) 海南省自然科学基金(20158332) 三亚市医疗卫生科技创新项目(2014YW33)
关键词 IGA肾病 IGA1 异常糖基化 免疫复合物 信号通路 IgA nephropathy IgA1 Abnormal glycosylation Immunocomplex Signaling pathway
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  • 1Jan Novak,Bruce A. Julian,Milan Tomana,Jiri Mestecky.??Progress in Molecular and Genetic Studies of IgA Nephropathy(J)Journal of Clinical Immunology . 2001 (5)
  • 2Reily C,Yamada K,Huang ZQ,et al.Abnormal STAT3 signaling enhances production of autoantigen in an autoimmune disease,Ig A nephropathy(Abstract)Journal of the American Society of Nephrology . 2013
  • 3Otani Masako,Nakata Junichiro,Kihara Masao,Leroy Valérie,Moll Solange,Wada Yoshinao,Izui Shozo.O-glycosylated IgA rheumatoid factor induces IgA deposits and glomerulonephritis. Journal of the American Society of Nephrology : JASN . 2011
  • 4Chan Loretta Y Y,Leung Joseph C K,Tsang Anita W L,Tang Sydney C W,Lai Kar Neng.Activation of tubular epithelial cells by mesangial-derived TNF-alpha: glomerulotubular communication in IgA nephropathy. Kidney International . 2005
  • 5Lai Kar Neng,Tang Sydney C W,Guh Jinn-Yuh,Chuang Tsai-Der,Lam Man Fai,Chan Loretta Y Y,Tsang Anita W L,Leung Joseph C K.Polymeric IgA1 from patients with IgA nephropathy upregulates transforming growth factor-beta synthesis and signal transduction in human mesangial cells via the renin-angiotensin system. Journal of the American Society of Nephrology : JASN . 2003
  • 6Suzuki H,Raska M,Yamada K,et al.Cytokines alter IgA1 O-glycosylation by dysregulating C1GalT1 and ST6GalNAc-IIenzymes. Journal of Biological Chemistry . 2014
  • 7Roos Anja,Rastaldi Maria Pia,Calvaresi Novella,Oortwijn Beatrijs D,Schlagwein Nicole,van Gijlswijk-Janssen Danielle J,Stahl Gregory L,Matsushita Misao,Fujita Teizo,van Kooten Cees,Daha Mohamed R.Glomerular activation of the lectin pathway of complement in IgA nephropathy is associated with more severe renal disease. Journal of the American Society of Nephrology : JASN . 2006
  • 8Xin G,Shi W,Xu LX,et al.Serum BAFF is elevated in patients with IgA nephropathy and associated with clinical and histopathological features. Journal of Nephrology . 2013
  • 9Suzuki H,Moldoveanu Z,Hall S,et al.Cytokines regulate aberrant glycosylation of Ig A1 in cell lines from patients with Ig A nephropathy(Abstract)Journal of the American Society of Nephrology . 2007
  • 10Yamada K,Huang ZQ,Raska M,et al.Effects of leukemia inhibitory factor and oncostatin M on Ig A1-producing cells from patients with Ig A nephropathy(Abstract)Journal of the American Society of Nephrology . 2012

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