防止线粒体反向电子传递作为心脏保护策略。

IF 7.5 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Basic Research in Cardiology Pub Date : 2023-08-28 DOI:10.1007/s00395-023-01002-4

Hiran A Prag, Michael P Murphy, Thomas Krieg

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引用次数: 2

摘要

在心肌梗死的情况下，线粒体复合体I上逆电子传递(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，我们概述了复合体I的RET产生超氧化物的必要条件以及它如何在再灌注过程中发生。此外，我们探索了与RET发生条件产生有关的各种途径，并提出了针对RET的潜在治疗策略，旨在实现心脏保护。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Preventing mitochondrial reverse electron transport as a strategy for cardioprotection.

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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 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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来源期刊

Basic Research in Cardiology 医学-心血管系统

CiteScore

16.30

自引率

5.30%

发文量

审稿时长

6-12 weeks

期刊介绍： Basic Research in Cardiology is an international journal for cardiovascular research. It provides a forum for original and review articles related to experimental cardiology that meet its stringent scientific standards. Basic Research in Cardiology regularly receives articles from the fields of - Molecular and Cellular Biology - Biochemistry - Biophysics - Pharmacology - Physiology and Pathology - Clinical Cardiology