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Updated: May 27, 2025

Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
Published on: July 3, 2018
The role of physical exercise in modulating microRNAs expression in acute myocardial infarction: a review
Raphael Furtado Marques1, Marcelo Souza de Andrade2,3, Andressa Coelho Ferreira2
1Northeast Biotechnology Network Postgraduate Program (RENORBIO), Federal University of Maranhão, São Luís, MA, Brazil. marques.raphaf@gmail.com.
Abstract:
MicroRNAs (miRNAs) have emerged as promising tools for diagnosis and treatment in numerous pathophysiological processes, including cardiovascular diseases (CVD). In this context, acute myocardial infarction (AMI) is one of the leading causes of death by CVD worldwide. In this sense, physical exercise (PE) is considered a non-pharmacological strategy to reduce the complex alterations in AMI. This study is an integrative review of the literature to explore the effects of PE on the cardiomyocyte post-AMI, including an understanding of the mechanisms by which the PE acts on the miRNAs expression. A review was performed on PubMed, Scopus, and Web of Science. After the searches, all records were imported into the Mendeley software, and duplicate articles were removed. The year of publication of the papers was not limited. 19 studies were performed on animal models, 10 in experimental models using rats, and 08 in models with mice and only one study was carried out on patients with AMI. The results showed the potential use of miRNAs as diagnostic tools and attractive biomarkers for treating AMI. In addition, PE can regulate miRNAs expression in the myocardial cell, promotes apoptosis resistance, autophagy regulation, lower cardiac fibrosis and cardiac hypertrophy, and higher angiogenesis through the signaling of miRNAs. The main microRNAs mitigating the deleterious effects of AMI and modulated by PE were miRNA-222, miRNA-1192, miRNA-146, and miRNA-126. PE modulates the expression of specific miRNAs that support cardiac function, promoting cardioprotective effects or facilitating cardiac recovery post-AMI.
Insights
Physical exercise (PE) influences microRNAs (miRNAs) to aid recovery after acute myocardial infarction (AMI). PE regulates specific miRNAs, offering cardioprotective effects and improving cardiac function post-AMI.
Area of Science:
- Cardiology
- Molecular Biology
- Exercise Physiology
Background:
- Cardiovascular diseases (CVD), particularly acute myocardial infarction (AMI), represent a major global health concern.
- MicroRNAs (miRNAs) are emerging as critical regulators in various pathophysiological processes, including CVD.
- Physical exercise (PE) is a recognized non-pharmacological intervention for managing AMI complications.
Purpose of the Study:
- To conduct an integrative literature review on the effects of PE on cardiomyocyte function post-AMI.
- To elucidate the mechanisms through which PE modulates miRNA expression in the context of AMI.
- To identify specific miRNAs influenced by PE that contribute to cardiac recovery.
Main Methods:
- An integrative literature review was performed using PubMed, Scopus, and Web of Science databases.
- Studies included animal models (rats, mice) and a limited number of human studies on AMI patients.
- Data extraction and synthesis were conducted, with duplicate articles removed using Mendeley software.
Main Results:
- miRNAs show potential as diagnostic tools and therapeutic biomarkers for AMI.
- PE effectively regulates miRNA expression in myocardial cells, promoting apoptosis resistance and autophagy.
- PE was found to reduce cardiac fibrosis and hypertrophy while enhancing angiogenesis via miRNA signaling.
Conclusions:
- Specific miRNAs, including miRNA-222, miRNA-1192, miRNA-146, and miRNA-126, are key in mitigating AMI's adverse effects and are modulated by PE.
- PE's modulation of these miRNAs supports cardiac function, offering cardioprotective benefits and facilitating recovery after AMI.
- miRNAs represent a significant molecular pathway through which PE exerts its beneficial effects on the post-infarcted heart.

