Journal
CURRENT OPINION IN CELL BIOLOGY
Volume 22, Issue 2, Pages 177-180Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2009.11.015
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Funding
- Ligue Nationale Contre le Cancer (Equipe labellisee LNCC)
- Association pour la Recherche contre le Cancer (ARC)
- Agence Nationale pour la Recherche (ANR)
- National Cancer Institute (INCa)
- METOXIA (EU)
- Centre A. Lacassagne
- University of Nice
- CNRS
- INSERM
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Hypoxia (similar to 3-0.1% oxygen) is capable of rapidly inducing, via the hypoxia-inducible factor (HIF-1), a cell survival response engaging autophagy. This process is mediated by the atypical BH3-only proteins the Bcl-2/E1B 19 kDa-interacting protein 3 (BNIP3/BNIP3L (NIX)) that are induced by HIF-1. These mitochondria! associated BNIP proteins also mediate mitophagy, a metabolic adaptation for survival that is able to control reactive oxygen species (ROS) production and DNA damage. In contrast, severe hypoxic conditions or anoxia (<0.1% oxygen), where the latter is often confused with physiological hypoxia, are capable of inducing a HIF-independent autophagic response, generated via an extreme nutritional stress response implicating the AMPK-mTOR and unfolded protein response (UPR) pathways. The autophagic cell death that is often observed in these extreme stress conditions should be seen as the outcome of failed adaptation.
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