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Article Addendum

Mitochondrial autophagy: Life and breath of the cell

Gregg L. Semenza

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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 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.

Addendum to: Zhang H, Bosch-Marce M, Shimoda LA, Tan YS, Baek JH, Wesley JB, Gonzalez FJ, Semenza GL. Mitochondrial autophagy is a HIF-1-dependent adaptive metabolic response to hypoxia. J Biol Chem 2008; In press.

Authors

Gregg L. Semenza

The Johns Hopkins University School of Medicine

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