Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review).

Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review).
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DOI:
10.3892/etm.2022.11357
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发表时间:
2022-06
影响因子:
2.7
通讯作者:
--
中科院分区:
医学4区
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--
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心肌梗死是全球冠心病患者死亡的主要原因之一。急性心肌梗死的早期治疗可恢复缺血心肌的血供,降低死亡风险。然而,当中断的心肌血供在一定时间内恢复时,会对原有缺血心肌造成更严重的损害;这被称为心肌缺血/再灌注损伤(MIRI)。MIRI的病理生理机制与氧化应激、细胞内钙超载、能量代谢紊乱、细胞凋亡、内质网应激、自噬、焦亡、坏死凋亡和铁亡有关。这些因素相互作用,直接或间接地导致影响的加重。在过去,细胞凋亡和自噬引起了更多的关注,但坏死性凋亡和铁凋亡也发挥了关键作用。然而,MIRI的机制尚未完全阐明。本文就MIRI的机制作一综述。基于目前对MIRI病理生理机制的理解,阐述了细胞死亡相关信号通路之间的关联,为临床治疗中寻找新靶点提供了方向。
Myocardial infarction is one of the primary causes of mortality in patients with coronary heart disease worldwide. Early treatment of acute myocardial infarction restores blood supply of ischemic myocardium and decreases the mortality risk. However, when the interrupted myocardial blood supply is recovered within a certain period of time, it causes more serious damage to the original ischemic myocardium; this is known as myocardial ischemia/reperfusion injury (MIRI). The pathophysiological mechanisms leading to MIRI are associated with oxidative stress, intracellular calcium overload, energy metabolism disorder, apoptosis, endoplasmic reticulum stress, autophagy, pyroptosis, necroptosis and ferroptosis. These interplay with one another and directly or indirectly lead to aggravation of the effect. In the past, apoptosis and autophagy have attracted more attention but necroptosis and ferroptosis also serve key roles. However, the mechanism of MIRI has not been fully elucidated. The present study reviews the mechanisms underlying MIRI. Based on current understanding of the pathophysiological mechanisms of MIRI, the association between cell death-associated signaling pathways were elaborated, providing direction for investigation of novel targets in clinical treatment.
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