Podocyte Biology and Pathogenesis of Kidney Disease

被引：168

作者：

Reiser, Jochen ^{[1
]}

Sever, Sanja ^{[2
,3
]}

机构：

[1] Rush Univ, Med Ctr, Dept Med, Chicago, IL 60612 USA

[2] Massachusetts Gen Hosp, Div Nephrol, Charlestown, MA 02129 USA

[3] Harvard Univ, Sch Med, Charlestown, MA 02129 USA

来源：

ANNUAL REVIEW OF MEDICINE, VOL 64 | 2013年 / 64卷

关键词：

CKD; actin cytoskeleton; dynamin; suPAR; novel therapeutics; CATHEPSIN-L; DYNAMIN; PROTEINURIA; MECHANISMS; EXPRESSION; NEPHRIN; TARGET;

D O I：

10.1146/annurev-med-050311-163340

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Proteinuric chronic kidney disease (CKD), once a rare affliction believed to be mainly caused by genetic mutations, has become a global pandemic that severely diminishes the quality of life for millions. Despite the changing face of CKD, treatment options and resources remain woefully antiquated and have failed to arrest or reverse the effects of kidney-related diseases. Histological and genetic data strongly implicate one promising target: the podocyte. Podocytes are terminally differentiated cells of the kidney glomerulus that are essential for the integrity of the kidney filter. Their function is primarily based on their intricate structure, which includes foot processes. Loss of these actin-driven membrane extensions is tightly connected to the presence of protein in the urine, podocyte loss, development of CKD, and ultimately renal failure.

引用

页码：357 / 366

页数：10

共 36 条

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