Du Bingxin, Fu Qiang, Yang Qin, Yang Yeying, Li Rui, Yang Xu, Yang Qingrong, Li Shuo, Tian Jinwei, Liu Huibin
Department of Pharmacy, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Department of Chinese Formulae, Heilongjiang University of Chinese Medicine, Harbin, China.
Cell Death Discov. 2025 Mar 5;11(1):87. doi: 10.1038/s41420-025-02372-5.
Myocardial ischemia-reperfusion (I/R) injury is a multifaceted process observed in patients with coronary artery disease when blood flow is restored to the heart tissue following ischemia-induced damage. Cardiomyocyte cell death, particularly through apoptosis, necroptosis, autophagy, pyroptosis, and ferroptosis, is pivotal in myocardial I/R injury. Preventing cell death during the process of I/R is vital for improving ischemic cardiomyopathy. These multiple forms of cell death can occur simultaneously, interact with each other, and contribute to the complexity of myocardial I/R injury. In this review, we aim to provide a comprehensive summary of the key molecular mechanisms and regulatory patterns involved in these five types of cell death in myocardial I/R injury. We will also discuss the crosstalk and intricate interactions among these mechanisms, highlighting the interplay between different types of cell death. Furthermore, we will explore specific molecules or targets that participate in different cell death pathways and elucidate their mechanisms of action. It is important to note that manipulating the molecules or targets involved in distinct cell death processes may have a significant impact on reducing myocardial I/R injury. By enhancing researchers' understanding of the mechanisms and interactions among different types of cell death in myocardial I/R injury, this review aims to pave the way for the development of novel interventions for cardio-protection in patients affected by myocardial I/R injury.
心肌缺血再灌注(I/R)损伤是一个多方面的过程,在冠心病患者中,当缺血性损伤后心脏组织血流恢复时可观察到。心肌细胞死亡,特别是通过凋亡、坏死性凋亡、自噬、焦亡和铁死亡,在心肌I/R损伤中起关键作用。在I/R过程中预防细胞死亡对于改善缺血性心肌病至关重要。这些多种形式的细胞死亡可同时发生、相互作用,并导致心肌I/R损伤的复杂性。在本综述中,我们旨在全面总结心肌I/R损伤中这五种类型细胞死亡所涉及的关键分子机制和调控模式。我们还将讨论这些机制之间的相互作用和复杂的交互作用,突出不同类型细胞死亡之间的相互影响。此外,我们将探索参与不同细胞死亡途径的特定分子或靶点,并阐明其作用机制。需要注意的是,操纵参与不同细胞死亡过程的分子或靶点可能对减少心肌I/R损伤有重大影响。通过增强研究人员对心肌I/R损伤中不同类型细胞死亡的机制及相互作用的理解,本综述旨在为受心肌I/R损伤影响的患者开发新型心脏保护干预措施铺平道路。