The pluripotent role of exosomes in mediating non-coding RNA in ventricular remodeling after myocardial infarction.

With the increase of an aging population and the rising incidence of cardiovascular diseases, heart failure (HF) patients are on the rise every year. Myocardial infarction (MI) is the leading cause of HF in patients among cardiovascular diseases. In clinic, patients with MI are often assessed by biochemical indicators, electrocardiography, brain natriuretic peptide levels, myocardial enzymology, echocardiography and other means to predict the occurrence of HF and ventricular remodeling (VR). But there is still a lack of more accurate evaluation. VR is the basic mechanism of HF. In recent years, the molecular mechanism of VR has been studied mainly from the aspects of myocardial hypertrophy, myocardial fibrosis, inflammation, myocardial energy disorder, apoptosis, autophagy and pyroptosis. Exosomes are considered as the main mediators of intercellular information transmission. In addition, exosomes can promote the migration and transformation of intercellular RNAs, which are highly conserved non-coding RNAs. They can mediate the process of cell proliferation and differentiation of the target cell membrane. Exosomes have protective effects on VR after MI by inhibiting fibrosis, promoting angiogenesis and inhibiting inflammation and pyroptosis. We reviewed the specific protective mechanisms of exosomes for VR after MI. In addition, we discussed the formation of targeted exosomes and the role of non-coding RNAs in VR.