期刊
AUTOPHAGY
卷 4, 期 4, 页码 534-536出版社
LANDES BIOSCIENCE
DOI: 10.4161/auto.5956
关键词
mitochondrial autophagy; HIF-1; hypoxia; respiration; reactive oxygen species
类别
资金
- NHLBI NIH HHS [R01 HL055338-13, R01 HL055338-12, R01 HL055338-11, R01 HL055338-10A1] Funding Source: Medline
Homeostatic responses to reduced 02 availability are regulated by the transcriptional activator hypoxia-inducible factor I (HIF-1) in all metazoan species. An essential adaptation to sustained hypoxia is an active repression of mitochondrial respiration. In mouse embryo fibroblasts, HIF-1 induces expression of BNIP3, which triggers selective mitochondrial autophagy, When exposed to hypoxia, HIF-1-deficient cells do not induce BNIP3 or autophagy, do not decrease mitochondrial mass or downregulate respiration, and die within 72 hours due to toxic levels of reactive oxygen species. These studies indicate that mitochondrial. autophagy represents an adaptive metabolic response to hypoxia that is necessary to maintain redox homeostasis and cell survival.
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