本综述总结了活性氧在心肌缺血/再灌注损伤和心脏保护中的有益和有害作用。在第一部分中，强调了除了急性心肌梗塞快速再灌注之外对心脏保护的持续需求。然后，对心肌和冠状循环的心肌缺血/再灌注的病理机制以及心肌梗塞中细胞死亡的不同模式进行了表征。详细介绍了在选择性经皮冠状动脉介入治疗和冠状动脉旁路移植术、急性心肌梗塞和癌症治疗引起的心脏毒性中保护缺血/再灌注心肌的不同机械和药物干预措施。第二部分重点关注 ROS，全面概述缺血/再灌注损伤中涉及的分子和细胞机制。从线粒体作为缺血/再灌注心肌中 ROS 的主要来源和靶标开始，讨论了细胞和细胞外过程的复杂网络，包括与 Ca2 稳态的关系、硫醇基氧化还原平衡、硫化氢调节、与 NAPDH 氧化酶的串扰、外泌体、细胞因子和生长因子。虽然需要机制见解来改进我们当前的治疗方法，但 ROS 介导过程知识的进步表明，氧化应激的有害方面与生理和保护反应所需的 ROS 相对立。这种不可避免的对比可能会导致临床试验不成功，并限制仅仅基于 ROS 去除的新型心脏保护干预措施的开发。版权所有 © 2023 作者。由 Elsevier B.V. 出版。保留所有权利。

The present review summarizes the beneficial and detrimental roles of reactive oxygen species in myocardial ischemia/reperfusion injury and cardioprotection. In the first part, the continued need for cardioprotection beyond that by rapid reperfusion of acute myocardial infarction is emphasized. Then, pathomechanisms of myocardial ischemia/reperfusion to the myocardium and the coronary circulation and the different modes of cell death in myocardial infarction are characterized. Different mechanical and pharmacological interventions to protect the ischemic/reperfused myocardium in elective percutaneous coronary interventions and coronary artery bypass grafting, in acute myocardial infarction and in cardiotoxicity from cancer therapy are detailed. The second part keeps the focus on ROS providing a comprehensive overview of molecular and cellular mechanisms involved in ischemia/reperfusion injury. Starting from mitochondria as the main sources and targets of ROS in ischemic/reperfused myocardium, a complex network of cellular and extracellular processes is discussed, including relationships with Ca2+ homeostasis, thiol group redox balance, hydrogen sulfide modulation, cross-talk with NAPDH oxidases, exosomes, cytokines and growth factors. While mechanistic insights are needed to improve our current therapeutic approaches, advancements in knowledge of ROS-mediated processes indicate that detrimental facets of oxidative stress are opposed by ROS requirement for physiological and protective reactions. This inevitable contrast is likely to underlie unsuccessful clinical trials and limits the development of novel cardioprotective interventions simply based upon ROS removal.Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.