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.

中文翻译：

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防止线粒体反向电子传递作为心脏保护策略

在心肌梗塞的情况下，线粒体复合物 I 处的反向电子传递 (RET) 产生的超氧化物爆发是缺血/再灌注 (I/R) 损伤过程中损伤的关键触发因素。在这里，我们概述了 RET 在复合物 I 上产生超氧化物的必要条件以及在再灌注过程中如何发生超氧化物。此外，我们探索了与产生 RET 发生条件有关的各种途径，并提出了针对 RET 的潜在治疗策略，旨在实现心脏保护。