Key Laboratory of Medical Electrophysiology of the Ministry of Education, Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan, People's Republic of China.
Department of Cardiology, the Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People's Republic of China.
Int J Nanomedicine. 2024 Oct 19;19:10605-10621. doi: 10.2147/IJN.S476995. eCollection 2024.
Recanalization therapy can significantly improve the prognosis of patients with acute myocardial infarction (AMI). However, infarction or reperfusion-induced cardiomyocyte death, immune cell infiltration, fibroblast proliferation, and scarring formation lead to cardiac remodeling and gradually progress to heart failure or arrhythmia, resulting in a high mortality rate. Due to the inability of cardiomyocytes to regenerate, the healing of infarcted myocardium mainly relies on the formation of scars. Cardiac fibroblasts, as the main effector cells involved in repair and scar formation, play a crucial role in maintaining the structural integrity of the heart after MI. Recent studies have revealed that exosome-mediated intercellular communication plays a huge role in myocardial repair and signaling transduction after myocardial infarction (MI). Exosomes can regulate the biological behavior of fibroblasts by activating or inhibiting the intracellular signaling pathways through their contents, which are derived from cardiomyocytes, immune cells, endothelial cells, mesenchymal cells, and others. Understanding the interactions between fibroblasts and other cell types during cardiac remodeling will be the key to breakthrough therapies. This review examines the role of exosomes from different sources in the repair process after MI injury, especially the impacts on fibroblasts during myocardial remodeling, and explores the use of exosomes in the treatment of myocardial remodeling after MI.
再灌注治疗可显著改善急性心肌梗死（AMI）患者的预后。然而，梗死或再灌注诱导的心肌细胞死亡、免疫细胞浸润、成纤维细胞增殖和瘢痕形成导致心脏重构，并逐渐进展为心力衰竭或心律失常，导致死亡率较高。由于心肌细胞不能再生，梗死心肌的愈合主要依赖于瘢痕的形成。心肌细胞损伤后，心肌修复和重塑的主要细胞包括心肌细胞、成纤维细胞、血管内皮细胞、免疫细胞等。心脏成纤维细胞作为参与修复和瘢痕形成的主要效应细胞，在 MI 后维持心脏的结构完整性方面发挥着重要作用。最近的研究表明，外泌体介导的细胞间通讯在心肌梗死后的心肌修复和信号转导中起着巨大的作用。外泌体可以通过其内容物激活或抑制细胞内信号通路，从而调节成纤维细胞的生物学行为，这些内容物来源于心肌细胞、免疫细胞、内皮细胞、间充质细胞等。了解心脏重构过程中成纤维细胞与其他细胞类型之间的相互作用将是突破治疗的关键。本综述探讨了不同来源的外泌体在 MI 损伤后修复过程中的作用，特别是对心肌重塑过程中成纤维细胞的影响，并探讨了外泌体在 MI 后心肌重塑治疗中的应用。
