Li J J, Kwak S J, Jung D S, Kim J-J, Yoo T-H, Ryu D-R, Han S H, Choi H Y, Lee J E, Moon S J, Kim D K, Han D S, Kang S-W
Department of Internal Medicine, Nephrology and Dialysis Unit, The Affiliated Hospital, YanBian University Medical College, JiLin, China.
Kidney Int Suppl. 2007 Aug(106):S36-42. doi: 10.1038/sj.ki.5002384.
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.
肾小球脏层上皮细胞，即足细胞，是高度特化的细胞，可产生初级突起、次级突起，最终形成足突。相邻足细胞的足突相互交错，其间留有滤过裂隙。这些裂隙由一种称为裂孔隔膜的细胞外物质连接，裂孔隔膜在建立防止蛋白质丢失的大小选择性屏障中起主要作用。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、巢蛋白和集聚蛋白。由于糖尿病肾病的临床特征为蛋白尿，病理特征为肾小球肥大、GBM增厚伴足突消失，足细胞一直是糖尿病肾病研究领域的焦点。因此，许多研究表明，糖尿病环境本身、血流动力学变化以及局部生长因子，如转化生长因子-β和血管紧张素II，这些被认为是糖尿病肾病发病机制中的介质，可直接和/或间接诱导足细胞肥大、凋亡和结构改变，并增加IV型胶原的合成。本综述探讨了糖尿病条件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。
