Mitochondrial autophagy is an HIF-1-dependent adaptive metabolic response to hypoxia

J Biol Chem. 2008 Apr 18;283(16):10892-903. doi: 10.1074/jbc.M800102200. Epub 2008 Feb 15.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Retracted Publication

MeSH terms

  • Animals
  • Apoptosis Regulatory Proteins
  • Autophagy*
  • Autophagy-Related Protein 5
  • Beclin-1
  • Cell Death
  • Cytoplasm / metabolism
  • Hypoxia*
  • Hypoxia-Inducible Factor 1 / metabolism*
  • Membrane Proteins / biosynthesis
  • Mice
  • Mice, Knockout
  • Microtubule-Associated Proteins / biosynthesis
  • Mitochondria / metabolism*
  • Mitochondrial Proteins / biosynthesis
  • Models, Biological
  • Molecular Conformation
  • Proteins / metabolism
  • Reactive Oxygen Species

Substances

  • Apoptosis Regulatory Proteins
  • Atg5 protein, mouse
  • Autophagy-Related Protein 5
  • BNip3 protein, mouse
  • Beclin-1
  • Becn1 protein, mouse
  • Hypoxia-Inducible Factor 1
  • Membrane Proteins
  • Microtubule-Associated Proteins
  • Mitochondrial Proteins
  • Proteins
  • Reactive Oxygen Species