足细胞
糖尿病肾病
医学
肾小球硬化
疾病
肾功能
肾病
肾脏疾病
肾小球
膜性肾病
肾小球肾炎
肾
内科学
癌症研究
生物信息学
蛋白尿
内分泌学
生物
糖尿病
作者
Sandeep K. Mallipattu,John Cijiang He
出处
期刊:American Journal of Physiology-renal Physiology
[American Physiological Society]
日期:2016-07-01
卷期号:311 (1): F46-F51
被引量:61
标识
DOI:10.1152/ajprenal.00184.2016
摘要
The Centers for Disease Control and Prevention estimates more than 10% of adults in the United States, over 20 million Americans, have chronic kidney disease (CKD). A failure to maintain the glomerular filtration barrier directly contributes to the onset of CKD. The visceral epithelial cells, podocytes, are integral to the maintenance of this renal filtration barrier. Direct podocyte injury contributes to the onset and progression of glomerular diseases such as minimal change disease (MCD), focal segmental glomerular sclerosis (FSGS), diabetic nephropathy, and HIV-associated nephropathy (HIVAN). Since podocytes are terminally differentiated with minimal capacity to self-replicate, they are extremely sensitive to cellular injury. In the past two decades, our understanding of the mechanism(s) by which podocyte injury occurs has greatly expanded. With this newfound knowledge, therapeutic strategies have shifted to identifying targets directed specifically at the podocyte. Although the systemic effects of these agents are important, their direct effect on the podocyte proves to be essential in ameliorating glomerular disease. In this review, we highlight the mechanisms by which these agents directly target the podocyte independent of its systemic effects.
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