Noncoding RNAs in myocardial ischemia/reperfusion injury and repair

IF 2.5 Q2 PHYSIOLOGY
Mingliang Pan , Zhixin Li , Xiaohong Wang , Liying Zhan , Guo-Chang Fan
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引用次数: 0

Abstract

Myocardial ischemia/reperfusion (I/R) usually triggers a series of molecular and cellular changes, which yield excessive oxidative stress and massive cardiomyocyte death, leading to sterile inflammation, cardiac fibrosis, and, eventually, heart failure. Over the past two decades, numerous studies have demonstrated that noncoding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), involve almost every aspect of adverse cardiac remodeling induced by I/R. They have emerged as key regulators in the process of cardiac cell death (i.e. apoptosis, necroptosis, ferroptosis, pyroptosis, and PANoptosis), fibrosis, angiogenesis, and immune responses during myocardial I/R. Herein, this review summarizes recent advancements on ncRNA-mediated regulation of cardiac cell death, cardiac angiogenesis, fibrosis, and macrophage function as well as intercellular communication following myocardial I/R. Finally, the therapeutic potential of ncRNAs for treating myocardial I/R injury and future research directions are also discussed.
非编码rna在心肌缺血/再灌注损伤及修复中的作用
心肌缺血/再灌注(I/R)通常会引发一系列分子和细胞变化,产生过度氧化应激和大量心肌细胞死亡,导致无菌炎症、心脏纤维化,最终导致心力衰竭。在过去的二十年中,大量研究表明,非编码rna (ncRNAs),包括microRNAs (miRNAs)、长链非编码rna (lncRNAs)和环状rna (circRNAs),几乎涉及I/R诱导的不良心脏重构的各个方面。在心肌I/R过程中,它们在心肌细胞死亡(即凋亡、坏死坏死、铁下垂、焦下垂和PANoptosis)、纤维化、血管生成和免疫反应过程中发挥关键调节作用。本文综述了心肌I/R后ncrna介导的心肌细胞死亡、血管生成、纤维化、巨噬细胞功能以及细胞间通讯调控的最新进展。最后,讨论了ncrna在心肌I/R损伤中的治疗潜力及未来的研究方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Current Opinion in Physiology
Current Opinion in Physiology Medicine-Physiology (medical)
CiteScore
5.80
自引率
0.00%
发文量
52
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