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Preventing mitochondrial reverse electron transport as a strategy for cardioprotection.

Published version
Peer-reviewed

Repository URI

https://www.repository.cam.ac.uk/handle/1810/356896

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Published version (6.43 MB)

Type

Article

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Authors

Prag, Hiran A  ORCID logo  https://orcid.org/0000-0002-4753-8567
Murphy, Michael P  ORCID logo  https://orcid.org/0000-0003-1115-9618
Krieg, Thomas  ORCID logo  https://orcid.org/0000-0002-5192-580X

Abstract

In the context of myocardial infarction, the burst of superoxide generated by reverse electron transport (RET) at complex I in mitochondria is a crucial trigger for damage during ischaemia/reperfusion (I/R) injury. Here we outline the necessary conditions for superoxide production by RET at complex I and how it can occur during reperfusion. In addition, we explore various pathways that are implicated in generating the conditions for RET to occur and suggest potential therapeutic strategies to target RET, aiming to achieve cardioprotection.

Description

Keywords

Malonate, Mitochondria, Reactive oxygen species, Reverse electron transport, Succinate, Succinate dehydrogenase, Humans, Electron Transport, Superoxides, Oxidative Phosphorylation, Mitochondria, Myocardial Infarction, Reperfusion Injury

Journal Title

Basic Res Cardiol

Conference Name

Journal ISSN

0300-8428
1435-1803

Volume Title

118

Publisher

Springer Science and Business Media LLC

Publisher DOI

https://doi.org/10.1007/s00395-023-01002-4

Rights and licensing

Attribution 4.0 International
Except where otherwised noted, this item's license is described as Attribution 4.0 International
Sponsorship
Medical Research Council (MC_UU_00015/3)
British Heart Foundation (PG/20/10025)
Wellcome Trust (220257/Z/20/Z)

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