A unifying mechanism for mitochondrial superoxide production during ischemia-reperfusion injury

Chouchani, E. T., Pell, V. R., James, A. M., Work, L. M. , Saeb-Parsy, K., Frezza, C., Krieg, T. and Murphy, M. P. (2016) A unifying mechanism for mitochondrial superoxide production during ischemia-reperfusion injury. Cell Metabolism, 23(2), pp. 254-263. (doi:10.1016/j.cmet.2015.12.009) (PMID:26777689)

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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.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Work, Dr Lorraine
Authors: Chouchani, E. T., Pell, V. R., James, A. M., Work, L. M., Saeb-Parsy, K., Frezza, C., Krieg, T., and Murphy, M. P.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
Journal Name:Cell Metabolism
Publisher:Elsevier (Cell Press)
ISSN:1550-4131
ISSN (Online):1932-7420
Published Online:14 January 2016
Copyright Holders:Copyright © 2016 Elsevier Inc.
First Published:First published in Cell Metabolism 23(2):254-263
Publisher Policy:Reproduced in accordance with the publisher copyright policy

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