Jin Chenyang, Ye Yutong, Gao Longzhe, Zhong Zikan, Zhou Changzuan, Wu Xiaoyu, Li Xudong, Zhou Genqing, Chen Songwen, Wei Yong, Cai Lidong, Liu Shaowen, Xu Juan
Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Cell Biosci. 2025 May 24;15(1):65. doi: 10.1186/s13578-025-01408-8.
Myocardial infarction (MI) is currently one of the most fatal cardiovascular diseases worldwide. The screening, treatment, and prognosis of MI are top priorities for cardiovascular centers globally due to its characteristic occult onset, high lethality, and poor prognosis. MI is caused by coronary artery occlusion induced by coronary atherosclerotic plaque blockage or other factors, leading to ischemic necrosis and apoptosis of cardiomyocytes. Although significant advancements have been made in the study of cardiomyocytes at the cellular and molecular levels, RNA-binding proteins (RBPs) have not been extensively explored in the context of MI. RBPs, as key regulators coordinating cell differentiation and tissue homeostasis, exhibit specific functions in gene transcription, RNA modification and processing, and post-transcriptional gene expression. By binding to their target RNA, RBPs coordinate various RNA dynamics, including cellular metabolism, subcellular localization, and translation efficiency, thereby controlling the expression of encoded proteins. Classical RBPs, including HuR, hnRNPs, and RBM family molecules, have been identified as critical regulators in myocardial hypoxia, oxidative stress, pro-inflammatory responses, and fibrotic repair. These RBPs exert their effects by modulating key pathophysiological pathways in MI, thereby influencing specific cardiac outcomes. Additionally, specific RBPs, such as QKI and fused in sarcoma (FUS), are implicated in the apoptotic pathways activated during MI. This apoptotic pathway represents a significant molecular phenotype in MI, offering novel perspectives and insights for mitigating cardiomyocyte apoptosis and attenuating the progression of MI. Therefore, this review systematically summarizes the role of RBPs in the main pathophysiological stages of MI and explores their potential therapeutic prospects.
心肌梗死（MI）是目前全球最致命的心血管疾病之一。由于其发病隐匿、致死率高和预后差的特点，MI的筛查、治疗和预后是全球心血管中心的首要任务。MI是由冠状动脉粥样硬化斑块阻塞或其他因素引起的冠状动脉闭塞所致，导致心肌细胞缺血坏死和凋亡。尽管在细胞和分子水平上对心肌细胞的研究取得了重大进展，但RNA结合蛋白（RBPs）在MI背景下尚未得到广泛探索。RBPs作为协调细胞分化和组织稳态的关键调节因子，在基因转录、RNA修饰和加工以及转录后基因表达中发挥特定功能。通过与靶RNA结合，RBPs协调各种RNA动态，包括细胞代谢、亚细胞定位和翻译效率，从而控制编码蛋白的表达。经典的RBPs，包括HuR、hnRNPs和RBM家族分子，已被确定为心肌缺氧、氧化应激、促炎反应和纤维化修复的关键调节因子。这些RBPs通过调节MI中的关键病理生理途径发挥作用，从而影响特定的心脏结局。此外，特定的RBPs，如QKI和肉瘤融合蛋白（FUS），与MI期间激活的凋亡途径有关。这种凋亡途径是MI中的一种重要分子表型，为减轻心肌细胞凋亡和减缓MI进展提供了新的视角和见解。因此，本综述系统总结了RBPs在MI主要病理生理阶段中的作用，并探讨了它们潜在的治疗前景。
