Pluijmert Niek J, Atsma Douwe E, Quax Paul H A
Department of Cardiology, Leiden University Medical Center, Leiden, Netherlands.
Department of Surgery, Leiden University Medical Center, Leiden, Netherlands.
Front Cardiovasc Med. 2021 Apr 28;8:647785. doi: 10.3389/fcvm.2021.647785. eCollection 2021.
Following acute occlusion of a coronary artery causing myocardial ischemia and implementing first-line treatment involving rapid reperfusion, a dynamic and balanced inflammatory response is initiated to repair and remove damaged cells. Paradoxically, restoration of myocardial blood flow exacerbates cell damage as a result of myocardial ischemia-reperfusion (MI-R) injury, which eventually provokes accelerated apoptosis. In the end, the infarct size still corresponds to the subsequent risk of developing heart failure. Therefore, true understanding of the mechanisms regarding MI-R injury, and its contribution to cell damage and cell death, are of the utmost importance in the search for successful therapeutic interventions to finally prevent the onset of heart failure. This review focuses on the role of innate immunity, chemokines, cytokines, and inflammatory cells in all three overlapping phases following experimental, mainly murine, MI-R injury known as the inflammatory, reparative, and maturation phase. It provides a complete state-of-the-art overview including most current research of all post-ischemic processes and phases and additionally summarizes the use of immunomodulatory therapies translated into clinical practice.
冠状动脉急性闭塞导致心肌缺血并实施包括快速再灌注的一线治疗后,会启动动态且平衡的炎症反应以修复和清除受损细胞。矛盾的是,心肌血流的恢复会因心肌缺血再灌注(MI-R)损伤而加剧细胞损伤,最终引发加速的细胞凋亡。最终,梗死面积仍与随后发生心力衰竭的风险相关。因此,真正理解MI-R损伤的机制及其对细胞损伤和细胞死亡的作用,对于寻找成功的治疗干预措施以最终预防心力衰竭的发生至关重要。本综述聚焦于天然免疫、趋化因子、细胞因子和炎症细胞在实验性(主要是小鼠)MI-R损伤后的三个重叠阶段(即炎症期、修复期和成熟期)中的作用。它提供了一个完整的最新概述,包括所有缺血后过程和阶段的最新研究,此外还总结了已转化为临床实践的免疫调节疗法的应用。