Key Takeaways & Executive Findings
- •• Specific miRNAs (e.g., miR-126, miR-29 family, miR-222) play critical roles in cardiac remodeling after acute myocardial infarction by targeting signaling pathways involved in angiogenesis, fibrosis, and calcium homeostasis, providing precise molecular targets for cardiac repair. • Exercise, as a non-pharmacological intervention, improves cardiac function after acute myocardial infarction by modulating miRNA expression, with mechanisms involving upregulation of miR-126, miR-29, miR-214-3p, and miR-222. • miRNAs exhibit dual roles as biomarkers and therapeutic targets in acute myocardial infarction, offering novel molecular tools for early diagnosis, efficacy monitoring, and prognosis assessment. • Combining exercise with pharmacological agents or nutrients (e.g., vitamin D3) can enhance the therapeutic effects of miRNA regulation, suggesting potential for integrated treatment strategies.
Abstract
BACKGROUND: The pathological manifestations of acute myocardial infarction primarily include cardiomyocyte apoptosis, fibrosis, impaired angiogenesis, calcium dyshomeostasis, and cardiac hypertrophy. MicroRNAs (miRNAs) are key regulators of gene expression and play significant roles in the progression of acute myocardial infarction. Exercise has been shown to improve cardiac function after acute myocardial infarction by modulating miRNA expression, although the underlying mechanisms remain incompletely understood. OBJECTIVE: To summarize the roles of miRNAs in the pathological features of acute myocardial infarction and discuss the molecular mechanisms through which exercise regulates miRNAs to treat acute myocardial infarction, thereby providing a theoretical reference for precise therapeutic interventions. METHODS: Literature published between 2000 and 2025 was retrieved from databases such as PubMed, Web of Science, CNKI, and Wanfang. Chinese search terms included 'acute myocardial infarction, cardiac remodeling, microRNA, myocardial cell apoptosis, myocardial fibrosis, angiogenesis, calcium homeostasis, cardiac hypertrophy, exercise'; English search terms included 'Acute Myocardial Infarction, Cardiac remodeling, MicroRNAs, Myocardial cell apoptosis, Myocardial fibrosis, Angiogenesis, Calcium homeostasis, Cardiac hypertrophy, Exercise'. A total of 92 articles were included for analysis. RESULTS AND CONCLUSION: miRNAs (miR-1, miR-133a, miR-21, miR-29 family) participate in cardiac remodeling after acute myocardial infarction by regulating signaling pathways related to apoptosis, fibrosis, angiogenesis, and calcium homeostasis. Exercise improves cardiac function after acute myocardial infarction by upregulating miR-126 to promote angiogenesis, upregulating miR-29 to inhibit myocardial fibrosis, upregulating miR-214-3p to restore calcium homeostasis, and upregulating miR-222 to promote physiological cardiac hypertrophy. Combination of exercise with drugs (e.g., trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl)urea) or nutrients (e.g., vitamin D3) can modulate the therapeutic effects of miRNAs. Future research should further investigate the spatiotemporal differences and inter-family differences of miRNAs to develop precise targeted intervention strategies; formulate precise exercise intervention plans based on miRNA expression profiles, combined with artificial intelligence for efficacy prediction and evaluation; and explore the combination of exercise intervention with gene editing or exosome delivery technologies to precisely regulate miRNA expression, thereby promoting cardiac repair and functional recovery.
1. Introduction
Acute myocardial infarction is a disease caused by sudden interruption of coronary blood flow, leading to myocardial ischemia and necrosis, and resulting in cardiac dysfunction [1-4]. miRNAs are non-coding RNAs of approximately 22 nucleotides in length that regulate gene expression by targeting the 3' untranslated region of messenger RNA, driving various biological processes such as cell proliferation, differentiation, and apoptosis [5]. Recent studies have found that miRNAs play important roles in acute myocardial infarction and cardiac repair. For example, miR-1 and miR-133a influence the extent of myocardial infarction and cardiac function by regulating cardiomyocyte apoptosis and differentiation [6]; miR-21 promotes cardiomyocyte survival and proliferation by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway [7]; and the miR-29 family alleviates cardiac fibrosis by inhibiting collagen synthesis [8]. However, the mechanisms of miRNAs in the treatment of acute myocardial infarction remain unclear.
Exercise has been widely used in the rehabilitation of acute myocardial infarction. Moderate exercise can improve cardiac function and quality of life in patients with acute myocardial infarction [9]. It is known that exercise can upregulate miR-126 to affect angiogenesis [10]; exercise can downregulate miR-15a and miR-146a to inhibit inflammatory responses [11-12]. However, the effects of different exercise types, intensities, and durations on miRNA expression are not uniform, and the clinical application potential of miRNAs as biomarkers for acute myocardial infarction requires further research support. Although there is a close relationship between exercise-induced improvement of cardiac function and miRNA regulation, the mechanisms by which exercise regulates miRNAs are not fully understood. Therefore, this review explores the roles of miRNAs in the pathological process of acute myocardial infarction and the regulatory mechanisms of exercise.
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Luan Chuankai, Zhu Lei (2026). Role and mechanism of exercise-regulated miRNAs in cardiac remodeling after acute myocardial infarction. Chinese Journal of Tissue Engineering Research. https://doi.org/10.12307/2026.21498
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Frequently Asked Questions
What is the role of miRNAs in cardiac remodeling after acute myocardial infarction?
miRNAs such as miR-1, miR-133a, miR-21, and the miR-29 family regulate key pathological processes including cardiomyocyte apoptosis, fibrosis, angiogenesis, and calcium homeostasis, thereby influencing cardiac remodeling after acute myocardial infarction.
How does exercise modulate miRNA expression to improve cardiac function after acute myocardial infarction?
Exercise upregulates specific miRNAs such as miR-126 (promoting angiogenesis), miR-29 (inhibiting fibrosis), miR-214-3p (restoring calcium homeostasis), and miR-222 (promoting physiological hypertrophy), collectively improving cardiac function.
Can exercise be combined with other treatments to enhance miRNA-based therapy for acute myocardial infarction?
Yes, combining exercise with drugs (e.g., trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl)urea) or nutrients (e.g., vitamin D3) can modulate the therapeutic effects of miRNAs, potentially leading to more effective treatment strategies.
What are the future directions for research on exercise-regulated miRNAs in acute myocardial infarction?
Future research should focus on understanding spatiotemporal and inter-family differences of miRNAs, developing precise exercise prescriptions based on miRNA expression profiles, integrating artificial intelligence for efficacy prediction, and exploring combination with gene editing or exosome delivery technologies for precise miRNA regulation.
What is the significance of miRNAs as biomarkers in acute myocardial infarction?
miRNAs have dual roles as biomarkers and therapeutic targets, offering potential for early diagnosis, monitoring of therapeutic efficacy, and prognosis assessment in acute myocardial infarction.
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