Targeting Succinate Metabolism in Ischemia/Reperfusion Injury.
Accepted version
Peer-reviewed
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Abstract
Timely reperfusion is critical for salvaging ischemic tissue in myocardial infarction, in stroke, and during resuscitation. Paradoxically, the reperfusion of blood into the ischemic organ is damaging in itself, leading to ischemia/reperfusion (IR) injury. Best clinical practice is to reperfuse rapidly to limit ischemic time. Despite this, extensive IR injury still occurs, which is a major driver of pathology, making the prevention of this damage a clear unmet clinical need.1 Recent work has shown a role for mitochondrial succinate metabolism in IR injury that opens up exciting new therapeutic approaches.
Description
Keywords
malonic acid, mitochondria, reactive oxygen species, succinic acid, Animals, Cardiotonic Agents, Humans, Reactive Oxygen Species, Reperfusion Injury, Succinate Dehydrogenase, Succinates, Time Factors
Journal Title
Circulation
Conference Name
Journal ISSN
0009-7322
1524-4539
1524-4539
Volume Title
140
Publisher
Ovid Technologies (Wolters Kluwer Health)
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All rights reserved
Sponsorship
Medical Research Council (MR/P000320/1)
British Heart Foundation (PG/15/84/31670)
British Heart Foundation (PG/15/84/31670)