Maintenance of redox homeostasis by hypoxia-inducible factors

Debangshu Samanta; Gregg L Semenza

doi:10.1016/j.redox.2017.05.022

Maintenance of redox homeostasis by hypoxia-inducible factors

Redox Biol. 2017 Oct:13:331-335. doi: 10.1016/j.redox.2017.05.022. Epub 2017 May 31.

Authors

Debangshu Samanta¹, Gregg L Semenza²

Affiliations

¹ McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205 USA; Johns Hopkins Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205 USA.
² McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205 USA; Johns Hopkins Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205 USA; Departments of Pediatrics, Medicine, Oncology, Radiation Oncology, and Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205 USA. Electronic address: gsemenza@jhmi.edu.

Abstract

Oxidative phosphorylation enables cells to generate the large amounts of ATP required for development and maintenance of multicellular organisms. However, under conditions of reduced O₂ availability, electron transport becomes less efficient, leading to increased generation of superoxide anions. Hypoxia-inducible factors switch cells from oxidative to glycolytic metabolism, to reduce mitochondrial superoxide generation, and increase the synthesis of NADPH and glutathione, in order to maintain redox homeostasis under hypoxic conditions.

Publication types

Review
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

Acetyl Coenzyme A / metabolism
Animals
Homeostasis*
Humans
Hypoxia-Inducible Factor 1 / genetics
Hypoxia-Inducible Factor 1 / metabolism*
Oxidative Stress*
Reactive Oxygen Species / metabolism
Signal Transduction

Substances

Hypoxia-Inducible Factor 1
Reactive Oxygen Species
Acetyl Coenzyme A