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线粒体自噬调控足细胞损伤的机制研究进展 被引量:1

Research progress on the mechanism of mitochondrial autophagy in regulating podocyte injury
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摘要 足细胞是维持肾小球功能的基本结构单位,对维持肾小球滤过作用具有关键意义。细胞自噬有助于维持足细胞的完整性。线粒体作为细胞供能的主要细胞器,对细胞生存与死亡起着重要调节作用。线粒体自噬作为一种特异性自噬,能够适时清除细胞内受损老化的线粒体,从而保证细胞内正常线粒体的数量和功能,对细胞的生长代谢起着重要作用。研究表明多种肾脏疾病中均出现足细胞损伤,同时伴有线粒体功能紊乱或细胞自噬异常等现象,足细胞线粒体自噬活动可通过PINK1/Parkin、Nrf2/Keap1等信号通路调控足细胞内环境稳态。本文总结线粒体和足细胞的生理病理表现,综述线粒体自噬稳态在足细胞病中作用的可能机制途径,有助于探索足细胞病新的治疗路径。 Podocytes are the basic structural unit for maintaining glomerular function,and are of crucial significance for maintaining glomerular filtration.Cellular autophagy helps maintain podocyte integrity.Mitochondria,as the main organelle for cell energy supply,play an important role in regulating cell survival and death.As a kind of specific autophagy,mitochondrial autophagy can timely remove damaged and aging mitochondria in cells,thereby ensuring the number and function of normal mitochondria in cells,and playing an important role in cell growth and metabolism.Studies have shown that podocyte damage occurs in a variety of kidney diseases,accompanied by mitochondrial dysfunction or abnormal cell autophagy.Podocyte mitochondrial autophagy activity can regulate the homeostasis of podocytes through signal pathways of PINK1/Parkin and Nrf2/Keap1,etc.This article summarized the physiopathological manifestations of mitochondria and podocytes,and reviewed the possible mechanisms of the role of mitochondrial autophagy homeostasis in podocyte disease,which might be helpful in exploring new therapeutic pathways for podocyte disease.
作者 魏丽凤 张先闻 王琳 Wei Lifeng;Zhang Xianwen;Wang Lin(Department of Nephrology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China)
出处 《中华肾病研究电子杂志》 2020年第6期275-278,共4页 Chinese Journal of Kidney Disease Investigation(Electronic Edition)
基金 国家自然科学基金项目(81273730) “陈以平全国名老中医工作室”多学科诊疗新模式建设与评价建设项目[ZY(2018-2020)-FWTX-6025] 上海市中医优势病种培育建设项目-尿酸性肾病[ZY(2018-2020)-ZYBZ-02]。
关键词 足细胞 线粒体自噬 稳态 调控 机制 Podocyte Mitochondrial autophagy Homeostasis Regulation Mechanism
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