Asanuma Katsuhiko
Kyoto University Graduate School of Medicine, TMK project, Medical Innovation Center.
Nihon Rinsho Meneki Gakkai Kaishi. 2015;38(1):26-36. doi: 10.2177/jsci.38.26.
It has recently become clear that initial glomerular injury affects glomerular visceral epithelial cells (also called as podocytes) as important target cells for progression of chronic kidney disease (CKD) and end-stage kidney disease. Podocytes are injured in many human kidney diseases including minimal change disease, focal segmental glomerulosclerosis, diabetic nephropathy, membranous nephropathy and lupus nephritis. 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 and an interposed slit-diaphragm. Chronic podocyte injury may cause podocyte detachment from the GBM, which leads to glomerulosclerosis. The elucidation of podocyte biology during the last 15 years has significantly improved our understanding of the pathophysiologic processes of proteinuria and glomerulosclerosis. In this review, we highlight some of new data including our recent findings for translating podocyte biology into new examinations and therapies for podocyte injury.
最近已经明确，最初的肾小球损伤会影响肾小球脏层上皮细胞（也称为足细胞），这些细胞是慢性肾脏病（CKD）和终末期肾病进展的重要靶细胞。在许多人类肾脏疾病中，包括微小病变肾病、局灶节段性肾小球硬化症、糖尿病肾病、膜性肾病和狼疮性肾炎，足细胞都会受到损伤。足细胞是高度特化的上皮细胞，覆盖在肾小球基底膜（GBM）的外层。足细胞通过足突的特殊形成和维持以及中间的裂孔隔膜，成为阻止尿蛋白丢失的最后一道屏障。慢性足细胞损伤可能导致足细胞与GBM分离，进而导致肾小球硬化。在过去15年中，对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。在这篇综述中，我们重点介绍一些新数据，包括我们最近关于将足细胞生物学转化为足细胞损伤新检查和治疗方法的研究结果。
