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Originally published In Press as doi:10.1074/jbc.M800102200 on February 15, 2008

J. Biol. Chem., Vol. 283, Issue 16, 10892-10903, April 18, 2008
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Mitochondrial Autophagy Is an HIF-1-dependent Adaptive Metabolic Response to Hypoxia*Formula

Huafeng Zhang{ddagger}§, Marta Bosch-Marce{ddagger}§, Larissa A. Shimoda, Yee Sun Tan{ddagger}§, Jin Hyen Baek{ddagger}§, Jacob B. Wesley{ddagger}§, Frank J. Gonzalez||, and Gregg L. Semenza{ddagger}§**{ddagger}{ddagger}§§1

From the {ddagger}Vascular Program, Institute for Cell Engineering, §McKusick-Nathans Institute of Genetic Medicine, and Department of Medicine, **Pediatrics, {ddagger}{ddagger}Oncology, and §§Radiation Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 and ||Laboratory of Metabolism, NCI, National Institutes of Health, Bethesda, Maryland 20892

Autophagy is a process by which cytoplasmic organelles can be catabolized either to remove defective structures or as a means of providing macromolecules for energy generation under conditions of nutrient starvation. In this study we demonstrate that mitochondrial autophagy is induced by hypoxia, that this process requires the hypoxia-dependent factor-1-dependent expression of BNIP3 and the constitutive expression of Beclin-1 and Atg5, and that in cells subjected to prolonged hypoxia, mitochondrial autophagy is an adaptive metabolic response which is necessary to prevent increased levels of reactive oxygen species and cell death.

Received for publication, January 4, 2008 , and in revised form, February 8, 2008.

* This work was supported by funds from the Johns Hopkins Institute for Cell Engineering and National Institutes of Health Public Health Service Grant P50-CA103175. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Formula The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. 1-6 and Tables 1 and 2.

1 To whom correspondence should be addressed: Broadway Research Bldg., Suite 671, 733 North Broadway, Baltimore, MD 21205. Fax: 443-287-5618; E-mail: gsemenza{at}jhmi.edu.


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