足细胞损伤发展为肾小球硬化的机制

K. Asanuma
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引用次数: 1

摘要

肾小球内脏上皮细胞,也被称为足细胞,是高度特化的上皮细胞,覆盖在肾小球基底膜(GBM)外层。足细胞通过特殊的足突(FPs)的形成和维持以及插入的狭缝隔膜(SD),作为尿蛋白流失的最终屏障。慢性足细胞损伤可引起足细胞脱离GBM,从而导致肾小球硬化。在过去的十年中足细胞生物学的阐明显著提高了我们对蛋白尿和肾小球硬化病理生理过程的理解。本文综述了足细胞生物学转化为足细胞损伤新疗法和检查的一些最新发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanism of the Progression from Podocyte Injury to Glomerulosclerosis
Glomerular visceral epithelial cells, also known as podocytes, are highly specialized epithelial cells that cover the outer layer of the glomerular basement membrane (GBM). Podocytes serve as the final barrier to urinary protein loss through the special formation and maintenance of foot processes (FPs) and an interposed slit diaphragm (SD). Chronic podocyte injury may cause podocyte detachment from the GBM, which leads to glomerulosclerosis. The elucidation of podocyte biology during the last decade has significantly improved our understanding of the pathophysiologic processes of proteinuria and glomerulosclerosis. This review highlights some of the recent findings for translating podocyte biology into new therapies and examinations for podocyte injury.
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