MicroRNAS AND PHYSICAL EXERCISE IN MYOCARDIAL INFARCTION: A REVIEW

INTRODUCTION: MicroRNAs (miRNAs) are small non-coding RNA molecules that post-transcriptionally modulate gene expression and have emerged as possible diagnostic and therapeutic targets for different cardiovascular diseases (CVD). In this CVD scenario, acute myocardial infarction (AMI) stands out, whose pathology involves apoptosis, fibrosis, and cardiac remodeling, which contribute to adverse cardiac outcomes. A non-pharmacological therapeutic measure to reduce complex AMI changes is exercise training (ET), which is used to improve cardiac function in post-AMI patients.  In this context, miRNAs stand out as markers of the effect of SSD after AMI. Therefore, this study aimed to investigate the effects promoted by TF on the myocardium, post-AMI, and to understand the mechanisms of action of TF on the expression of miRNAs in cardiomyocytes.  METHODS: The search was conducted in the Pubmed, Web of Science and Scopus repositories, resulting in 596 identified articles and 19 reviewed studies, which addressed the impact of TF on AMI markers correlated with miRNAs. RESULTS: The 19 studies reviewed used an animal model in rats and mice, and the main models of ET were performed on a treadmill and/or swimming. The studies report the potential of miRNAs as diagnostic tools and therapeutic targets in AMI and their participation in the regulatory pathway of SSD on the myocardium. The reviewed studies demonstrated that TF promotes regulation of the apoptosis and autophagy process through the regulation of miRNA-30d-5p, miRNA-34a, miRNA-125b, miRNA-128-3p miR-146-a, miRNA-208b, miRNA-222, miRNA-497 and miRNA-119, beyond the regulation of angiogenesis through miRNA-15a, miRNA-126, and miRNA-146a, the transcription factor (TF) also regulates cardiac hypertrophy via miRNA-222. Additionally, several studies have reported positive effects on calcium homeostasis through miRNA-1, miRNA-31a-5p, miRNA-133a, miR-140-3p and 5p, miR208a-3p and 5p, miRNA-214-3p, and miRNA-497-5p. CONCLUSION: The TF modulates the expression of specific miRNAs for myocardial function, favoring either cardioprotective effects or post-myocardial infarction (MI) cardiac recovery by reducing cardiac apoptosis and fibrosis, increasing angiogenesis, cardiac remodeling, and calcium modulation.