Fibrotic Changes Mediating Acute Kidney Injury to Chronic Kidney Disease Transition

被引：30

作者：

hAinmhire, Eoghainin O. ^{[1
]}

Humphreys, Benjamin D. ^{[1
]}

机构：

[1] Washington Univ, Sch Med, Div Nephrol, 660 S Euclid Ave,CB 8129, St Louis, MO 63110 USA

来源：

NEPHRON | 2017年 / 137卷 / 04期

关键词：

Acute renal failure; Fibrosis; Ischemia-reperfusion injury; NOTCH; FIBROSIS; ACTIVATION; PATHWAY; EXPRESSION; MOLECULE-1; REPAIR; PROGRESSION; RECEPTOR; MICE;

D O I：

10.1159/000474960

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

End-stage renal disease (ESRD) is common, costly, and it results from progressive chronic kidney disease (CKD). ESRD claims many lives every year. It is increasingly recognized that episodes of acute kidney injury (AKI) predispose to the future development of CKD and ESRD. While our understanding of the pathophysiology of the AKI to CKD transition is improving, there are no validated therapeutic strategies to prevent this transition. In this review, we summarize the recent progress made in defining the cellular and molecular events underlying the AKI to CKD transition and highlight potential therapeutic targets and strategies to reduce the incidence of CKD following AKI. (C) 2017 S. Karger AG, Basel

引用

页码：264 / 267

页数：4

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