Mitochondrial autophagy: Life and breath of the cell

Research output: Contribution to journalArticlepeer-review


Homeostatic responses to reduced O2 availability are regulated by the transcriptional activator hypoxia-inducible factor 1 (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 the 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.

Original languageEnglish (US)
Pages (from-to)534-536
Number of pages3
Issue number4
StatePublished - May 16 2008


  • HIF-1
  • Hypoxia
  • Mitochondrial autophagy
  • Reactive oxygen species
  • Respiration

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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