Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.
Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.
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DOI：
10.1016/j.redox.2023.102894
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发表时间：
2023-11
期刊：
影响因子：
11.4
通讯作者：
Di Lisa, Fabio
中科院分区：
文献类型：
--
作者：
Heusch, Gerd;Andreadou, Ioanna;Bell, Robert;Bertero, Edoardo;Botker, Hans-Erik;Davidson, Sean M.;Downey, James;Eaton, Philip;Ferdinandy, Peter;Gersh, Bernard J.;Giacca, Mauro;Hausenloy, Derek J.;Ibanez, Borja;Krieg, Thomas;Maack, Christoph;Schulz, Rainer;Sellke, Frank;Shah, Ajay M.;Thiele, Holger;Yellon, Derek M.;Di Lisa, Fabio
关键词：
本文综述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，强调了在急性心肌梗死快速再通之外对心脏保护的持续需要。然后，阐述了心肌缺血/再灌注对心肌和冠脉循环的作用机制以及心肌梗死时细胞死亡的不同方式。在选择性经皮冠状动脉介入治疗和冠状动脉旁路移植术、急性心肌梗死和癌症治疗的心脏毒性方面，详细介绍了不同的机械和药物干预措施以保护缺血/再灌注心肌。第二部分继续关注ROS，全面概述了参与缺血/再灌注损伤的分子和细胞机制。从线粒体作为缺血/再灌注心肌ROS的主要来源和靶点出发，讨论了细胞和细胞外过程的复杂网络，包括与Ca~(2+)稳态、硫醇基氧化还原平衡、硫化氢调节、与NAPDH氧化酶、外切体、细胞因子和生长因子的关系。虽然改善我们目前的治疗方法需要机制上的洞察力，但对ROS介导的过程的了解的进展表明，氧化应激的有害方面与ROS对生理和保护反应的要求相反。这种不可避免的对比很可能是不成功的临床试验的基础，并限制了仅基于清除ROS的新的心脏保护干预措施的发展。缺血性心脏病是全球最常见的死亡原因。缺血/再灌注是缺血性心脏病的基础。心脏保护可减少心肌梗死面积和冠状动脉微血管阻塞。ROS是心脏保护的信号和损伤的执行者。到目前为止，将心脏保护转化为临床益处一直是困难的。ROS在心脏保护中的作用仍然是矛盾的。
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. Ischemic heart disease is the most frequent cause of death worldwide. Ischemia/reperfusion is the substrate of ischemic heart disease. Cardioprotection reduces infarct size and coronary microvascular obstruction. ROS are signals of cardioprotection and executors of injury. Translation of cardioprotection to clinical benefits has been difficult so far. The role of ROS in cardioprotection remains ambivalent.
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DOI：
10.1016/s0022-5223(95)70228-8
发表时间：
1995-08-01
影响因子：
6
作者：
ABDELFATTAH, AS;DING, M;WECHSLER, AS
通讯作者：
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影响因子：
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影响因子：
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