ArticlePloS one2024
Aerobic exercise protects MI heart through miR-133a-3p downregulation of connective tissue growth factor.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanism study of miR-324-3p driving myocardial infarction progression through regulation of myocardial inflammation.Journal of cardiothoracic surgery · 2026Article
- MicroRNAs in Cardiovascular Diseases: Molecular Networks of Cellular Homeostasis, Inflammation, and Pathological Remodeling.International journal of molecular sciences · 2026Review
- Exercise-induced muscle exosomes: microRNA cargo as regulators of cardiovascular remodeling and disease progression.Journal of translational medicine · 2026Review
- Role of Copper Homeostasis and Cuproptosis in Cardiovascular Disease: Molecular Insights and Metabolic Perspectives.International journal of biological sciences · 2026Review
- Effects of Long-Term Moderate-Intensity Exercise on Autonomic Nervous System Dysfunction Induced by Cardiac Neurovascular Interface Deterioration.Reviews in cardiovascular medicine · 2025Review
- Comparison of Quercetin and Isoquercitrin's Anti-Heart Failure Activity via MAPK Inflammatory Pathway and Caspase Apoptosis Pathway.Pharmaceuticals (Basel, Switzerland) · 2025Article
- MicroRNAs at the crossroads of exercise and ferroptosis: a regulatory bridge.Clinical and experimental medicine · 2025Review
- Utilizing Circulating MicroRNAs for Personalized Exercise Programs: Insights into Physiological Adaptations and Individual Responses.Iranian journal of biotechnology · 2025Review
- Circulating extracellular vesicles regulate ELAVL1 by delivering miR-133a-3p which affecting NLRP3 mRNA stability inhibiting PANoptosome formation.Biology direct · 2025Article
- Altered Atlas of Exercise-Responsive MicroRNAs Revealing miR-29a-3p Attacks Armored and Cold Tumors and Boosts Anti-B7-H3 Therapy.Research (Washington, D.C.) · 2025Article
- Exercise mediates myocardial infarction via non-coding RNAs.Frontiers in cardiovascular medicine · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the effect of aerobic exercise intervention to inhibit cardiomyocyte apoptosis and thus improve cardiac function in myocardial infarction (MI) mice by regulating CTGF expression through miR-133a-3p.
methodsMale C57/BL6 mice, 7-8 weeks old, were randomly divided into sham-operated group (S group), sham-operated +aerobic exercise group (SE group), myocardial infarction group (MI group) and MI + aerobic exercise group (ME group). The mice were anesthetized the day after training and cardiac function was assessed by cardiac echocardiography. Myocardial collagen volume fraction (CVF%) was analyzed by Masson staining. Myocardial CTGF, Bax and Bcl-2 were detected by Western blotting, and myocardial miR-133a-3p was measured by RT-qPCR.
resultsCompared with the S group, miR-133a-3p, Bcl-2 and EF were significantly decreased and CTGF, Bax, Bax/ Bcl-2, Caspase 3, Cleaved Caspase-3, LVIDd, LVIDs and CVF were significantly increased in the MI group. Compared with the MI group, miR-133a-3p, Bcl-2 and EF were significantly increased, cardiac function was significantly improved, and CTGF, Bax, Bax/ Bcl-2, Caspase 3, Cleaved Caspase-3, LVIDd, LVIDs and CVF were significantly decreased in ME group. The miR-133a-3p was significantly lower and CTGF was significantly higher in the H2O2 intervention group compared with the control group of H9C2 rat cardiomyocytes. miR-133a-3p was significantly higher and CTGF was significantly lower in the AICAR intervention group compared to the H2O2 intervention group. Compared with the control group of H9C2 rat cardiomyocytes, CTGF, Bax and Bax/Bcl-2 were significantly increased and Bcl-2 was significantly decreased in the miR-133a-3p inhibitor intervention group; CTGF, Bax and Bax/Bcl-2 were significantly decreased and Bcl-2 was significantly upregulated in the miR-133a-3p mimics intervention group.
conclusionAerobic exercise down-regulated CTGF expression in MI mouse myocardium through miR-133a-3p, thereby inhibiting cardiomyocyte apoptosis and improving cardiac function.
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