Preventing mitochondrial reverse electron transport as a strategy for cardioprotection

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...

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Detalles Bibliográficos
Autores principales: Prag, Hiran A., Murphy, Michael P., Krieg, Thomas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2023
Materias:
Mitochondria at the Heart of Cardioprotection
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10462584/
https://www.ncbi.nlm.nih.gov/pubmed/37639068
http://dx.doi.org/10.1007/s00395-023-01002-4
Descripción
Sumario: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.

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