Journal
CELL CYCLE
Volume 7, Issue 9, Pages 1128-1132Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.7.9.5804
Keywords
hypoxia-inducible factor (HIF); hypoxia; chronic kidney disease; fibrosis; epithelial to mesenchymal transition (EMT); epithelial cell plasticity; lysyl oxidases
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Funding
- NCI NIH HHS [R01 CA100787] Funding Source: Medline
- NIDDK NIH HHS [R21 DK072037] Funding Source: Medline
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Capillary rarefaction is a hallmark of fibrotic diseases and results in reduced blood perfusion and oxygen delivery. In the kidney, tubulointerstitial fibrosis, which leads to the destruction of renal tissue and the irreversible loss of kidney function, is associated with hypoxia and the activation of Hypoxia-Inducible-Factor (HIF) signaling. HIF-1 and HIF-2 are basic-helix-loop-helix transcription factors that allow cells to survive in a low oxygen environment by regulating energy metabolism, vascular remodeling, erythropoiesis, cellular proliferation and apoptosis. Recent studies suggest that HIF activation promotes epithelial to mesenchymal transition (EMT) and renal fibrogenesis. These findings raise the possibility that the spectrum of HIF activated biological responses to hypoxic stress may differ under conditions of acute and chronic hypoxia. Here we discuss the role of HIF signaling in the pathogenesis and progression of chronic kidney disease.
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