Biology of Renal Recovery: Molecules, Mechanisms, and Pathways

被引：11

作者：

Vincent, Isaah S. ^{[1
]}

Okusa, Mark D. ^{[1
]}

机构：

[1] Univ Virginia Hlth Syst, Div Nephrol, Ctr Immun Inflammat & Regenerat Med, Charlottesville, VA USA

来源：

NEPHRON CLINICAL PRACTICE | 2014年 / 127卷 / 1-4期

基金：

美国国家卫生研究院;

关键词：

Acute kidney injury; Cell cycle; Fibrosis; Hypoxia-inducible factor-1 alpha; Inflammation; Mitochondria; ACUTE KIDNEY INJURY; MESENCHYMAL STEM-CELLS; MITOCHONDRIAL; FIBROSIS; PROTECT; REPAIR;

D O I：

10.1159/000363714

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：

Acute kidney injury (AKI) contributes to progressive kidney disease. Although significant advances have been made in the understanding of mechanisms of AKI, less is known about the biological basis that links the initial injury to progressive interstitial fibrosis, tubular dysfunction, and capillary rarefaction. The round table discussion focused on mechanisms of renal recovery and fibrosis following AKI. The knowledge gained by understanding these pathways will serve to identify novel therapeutic targets in the future. (C) 2014 S. Karger AG, Basel

引用

页码：10 / 14

页数：5

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