期刊
NEPHRON CLINICAL PRACTICE
卷 127, 期 1-4, 页码 10-14出版社
KARGER
DOI: 10.1159/000363714
关键词
Acute kidney injury; Cell cycle; Fibrosis; Hypoxia-inducible factor-1 alpha; Inflammation; Mitochondria
资金
- National Institutes of Health [R01 DK062324, R01 DK085259, T32 DK072922]
- NIH UAB-UCSD O'Brien Center [P30 DK079337]
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
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