Podocyte biology in diabetic nephropathy
Podocyte biology in diabetic nephropathy
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DOI：
10.1038/sj.ki.5002384
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发表时间：
2007-08-01
影响因子：
19.6
通讯作者：
Kang, S-W
中科院分区：
文献类型：
--
作者：
Li, J. J.;Kwak, S. J.;Kang, S-W
肾小球内脏上皮细胞，即足细胞，是高度特化的细胞，产生初级突起、次级突起，最后是足突。相邻足细胞的足突相互交错，在它们之间留下过滤缝隙。这些细胞外物质连接在一起，称为缝隙隔膜，它在建立蛋白质丢失的大小选择性屏障方面发挥着重要作用。此外，已知足细胞可合成肾小球基底膜(GBM)的基质分子，包括IV型胶原、层粘连蛋白、粘连蛋白和集聚蛋白。由于糖尿病肾病的临床特点是蛋白尿，病理表现为肾小球肥大、基底膜增厚伴足突消失，足细胞一直是糖尿病肾病研究领域的热点。因此，许多研究表明，糖尿病环境本身、血流动力学改变和局部生长因子如转化生长因子-β和血管紧张素Ⅱ等被认为是糖尿病肾病发病机制中的介质，直接和/或间接地诱导足细胞肥大、细胞凋亡和结构改变，并增加IV型胶原的合成。本文就糖尿病状态下足细胞的一些结构和功能变化及其在糖尿病肾病发生发展中的作用作一综述。
Glomerular visceral epithelial cells, namely podocytes, are highly specialized cells and give rise to primary processes, secondary processes, and finally foot processes. The foot processes of neighboring podocytes interdigitate, leaving between them filtration slits. These are bridged by an extracellular substance, known as the slit diaphragm, which plays a major role in establishing size-selective barrier to protein loss. Furthermore, podocytes are known to synthesize matrix molecules to the glomerular basement membrane (GBM), including type IV collagen, laminin, entactin, and agrin. Because diabetic nephropathy is clinically characterized by proteinuria and pathologically by glomerular hypertrophy and GBM thickening with foot process effacement, podocytes have been the focus in the field of research on diabetic nephropathy. As a result, many investigations have demonstrated that the diabetic milieu per se, hemodynamic changes, and local growth factors such as transforming growth factor-beta and angiotensin II, which are considered mediators in the pathogenesis of diabetic nephropathy, induce directly and/or indirectly hypertrophy, apoptosis, and structural changes, and increase type IV collagen synthesis in podocytes. This review explores some of the structural and functional changes of podocytes under diabetic conditions and their role in the development and progression of diabetic nephropathy.