期刊
NEPHRON CLINICAL PRACTICE
卷 127, 期 1-4, 页码 65-69出版社
KARGER
DOI: 10.1159/000363717
关键词
Acute kidney injury; Apoptosis; Cellular senescence; Epithelial cell injury; Fibrosis; Proximal tubule metabolism
资金
- NIH UAB-UCSD O'Brien Center [P30 DK079337]
- NIH [DK75976]
- Veterans Affairs Merit award
Fibrosis is a major hallmark of progressive kidney disease. The cellular mechanisms that lead to kidney tissue fibrosis are complex and include, for example, increased inflammation, increased oxidative stress, and proximal tubule cell death in the form of apoptosis or senescence. Recent studies have identified TWEAK, a tumor necrosis factor-like weak inducer of apoptosis, as a novel cytokine that mediates kidney inflammation in models of renal fibrosis. Inhibition of apoptosis via TWEAK inhibition has been shown to reduce kidney fibrosis. Recent studies using lineage tracing suggest that interstitial pericytes/perivascular fibroblasts differentiate into myofibroblasts and undergo proliferative expansion during fibrosis. Furthermore, increased expression of nuclear peroxisome proliferator-activated receptor-alpha in proximal tubules can directly reduce increased expression of transforming growth factor-beta 1 and interstitial inflammation in models of renal fibrosis, which suggests preservation of proximal tubule cell metabolism and integrity represents an important new therapeutic target. In this review, the current evidence and potential molecular mechanisms involved in the development of kidney fibrosis are discussed. (C) 2014 S. Karger AG, Basel
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