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A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury.


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Authors

Chouchani, Edward T 
Pell, Victoria R 
James, Andrew M 
Work, Lorraine M 
Saeb-Parsy, Kourosh  ORCID logo  https://orcid.org/0000-0002-0633-3696

Abstract

Ischemia-reperfusion (IR) injury occurs when blood supply to an organ is disrupted--ischemia--and then restored--reperfusion--leading to a burst of reactive oxygen species (ROS) from mitochondria. It has been tacitly assumed that ROS production during IR is a non-specific consequence of oxygen interacting with dysfunctional mitochondria upon reperfusion. Recently, this view has changed, suggesting that ROS production during IR occurs by a defined mechanism. Here we survey the metabolic factors underlying IR injury and propose a unifying mechanism for its causes that makes sense of the huge amount of disparate data in this area and provides testable hypotheses and new directions for therapies.

Description

Keywords

Animals, Electron Transport, Humans, Mitochondria, Models, Biological, Reperfusion Injury, Sulfhydryl Compounds, Superoxides

Journal Title

Cell Metab

Conference Name

Journal ISSN

1550-4131
1932-7420

Volume Title

23

Publisher

Elsevier BV
Sponsorship
Medical Research Council (MC_UU_12022/6)
MRC (unknown)
Medical Research Council (MC_U105663142)
Work in our laboratories is supported by the Medical Research Council (UK) and the British Heart Foundation. E.T.C. is supported by a Human Frontiers Science Program fellowship.