Cheng Peipei, Wang Xinting, Liu Qian, Yang Tao, Qu Huiyan, Zhou Hua
Institute of Cardiovascular Disease of Integrated Traditional Chinese and Western Medicine, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Branch of National Clinical Research Center for Chinese Medicine Cardiology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Front Pharmacol. 2023 Feb 22;14:1067992. doi: 10.3389/fphar.2023.1067992. eCollection 2023.
Acute myocardial infarction (AMI) is a severe ischemic disease with high morbidity and mortality worldwide. Maladaptive cardiac remodeling is a series of abnormalities in cardiac structure and function that occurs following myocardial infarction (MI). The pathophysiology of this process can be separated into two distinct phases: the initial inflammatory response, and the subsequent longer-term scar revision that includes the regression of inflammation, neovascularization, and fibrotic scar formation. Extracellular vesicles are nano-sized lipid bilayer vesicles released into the extracellular environment by eukaryotic cells, containing bioinformatic transmitters which are essential mediators of intercellular communication. EVs of different cellular origins play an essential role in cardiac remodeling after myocardial infarction. In this review, we first introduce the pathophysiology of post-infarction cardiac remodeling, as well as the biogenesis, classification, delivery, and functions of EVs. Then, we explore the dual role of these small molecule transmitters delivered by EVs in post-infarction cardiac remodeling, including the double-edged sword of pro-and anti-inflammation, and pro-and anti-fibrosis, which is significant for post-infarction cardiac repair. Finally, we discuss the pharmacological and engineered targeting of EVs for promoting heart repair after MI, thus revealing the potential value of targeted modulation of EVs and its use as a drug delivery vehicle in the therapeutic process of post-infarction cardiac remodeling.
急性心肌梗死（AMI）是一种严重的缺血性疾病，在全球范围内发病率和死亡率都很高。适应性不良的心脏重塑是心肌梗死（MI）后发生的一系列心脏结构和功能异常。这个过程的病理生理学可分为两个不同阶段：初始炎症反应，以及随后较长时期的瘢痕修复，包括炎症消退、新生血管形成和纤维化瘢痕形成。细胞外囊泡是真核细胞释放到细胞外环境中的纳米级脂质双层囊泡，含有生物信息传递分子，这些分子是细胞间通讯的重要介质。不同细胞来源的细胞外囊泡在心肌梗死后的心脏重塑中起重要作用。在这篇综述中，我们首先介绍梗死后心脏重塑的病理生理学，以及细胞外囊泡的生物发生、分类、传递和功能。然后，我们探讨这些由细胞外囊泡传递的小分子递质在梗死后心脏重塑中的双重作用，包括促炎和抗炎、促纤维化和抗纤维化的双刃剑作用，这对梗死后心脏修复具有重要意义。最后，我们讨论针对细胞外囊泡的药理学和工程靶向，以促进心肌梗死后的心脏修复，从而揭示靶向调控细胞外囊泡的潜在价值及其作为药物递送载体在梗死后心脏重塑治疗过程中的应用。
