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 > School of Cardiovascular & Metabolic Health |
| 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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