Cell-Autonomous Metabolic Reprogramming in Hypoxia

Luana Schito; Sergio Rey

doi:10.1016/j.tcb.2017.10.006

Cell-Autonomous Metabolic Reprogramming in Hypoxia

Trends Cell Biol. 2018 Feb;28(2):128-142. doi: 10.1016/j.tcb.2017.10.006. Epub 2017 Nov 27.

Authors

Luana Schito¹, Sergio Rey²

Affiliations

¹ Biological Sciences, Sunnybrook Research Institute, Toronto, ON M4N 3M5, Canada. Electronic address: luana.schito@ls2r.science.
² Princess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 1L7, Canada. Electronic address: sergio.rey@ls2r.science.

PMID: 29191366
DOI: 10.1016/j.tcb.2017.10.006

Abstract

Molecular oxygen (O₂) is a universal electron acceptor that enables ATP synthesis through mitochondrial respiration in all metazoans. Consequently, hypoxia (low O₂) has arisen as an organizing principle for cellular evolution, metabolism, and (patho)biology, eliciting a remarkable panoply of metabolic adaptations that trigger transcriptional, translational, post-translational, and epigenetic responses to determine cellular fitness. In this review we summarize current and emerging cell-autonomous molecular mechanisms that induce hypoxic metabolic reprogramming in health and disease.

Keywords: HIF; UPR; epigenetics; hypoxia; mTOR; metabolism.

Publication types

Review

MeSH terms

Animals
Cell Hypoxia / physiology
Cellular Reprogramming / physiology*
Energy Metabolism / physiology*
Humans
Oxygen / metabolism*
Signal Transduction / physiology

Substances

Oxygen