ArticleHypertension research : official journal of the Japanese Society of Hypertension2022
Mechanism of miR-378a-3p enriched in M2 macrophage-derived extracellular vesicles in cardiomyocyte pyroptosis after MI.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 28 citations in OpenAlex.
- Extracellular Vesicles in Cardiac Cell Crosstalk: from Intercellular Communication to Clinical Translation.Cardiovascular drugs and therapy · 2026Review
- Heterogeneity and Clinical Translation of Cardiac-Derived Extracellular Vesicles in Heart Failure: From Mechanisms to Precision Therapeutics.Reviews in cardiovascular medicine · 2026Review
- MicroRNAs in periodontal disease: from pathogenic mechanisms and RANKL/OPG regulation to nanoparticle delivery and personalized medicine.Frontiers in immunology · 2026Review
- Influenza-induced microRNA-155 expression is altered in extracellular vesicles derived from the COPD epithelium.Frontiers in cellular and infection microbiology · 2025Article
- Macrophage-driven exosomes regulate the progression of cardiovascular disease.Frontiers in pharmacology · 2025Review
- Extracellular vesicles in cardiovascular diseases: pathogenic mediators, diagnostic tools, and therapeutic vectors.Frontiers in cardiovascular medicine · 2025Review
- Large extracellular vesicles derived from LPS-preconditioned cardiomyocytes alleviate myocarditis via mediating macrophage polarization and modulating p38 MAPK pathway.Frontiers in immunology · 2025Article
- The interplay between T lymphocytes and macrophages in myocardial ischemia/reperfusion injury.Molecular and cellular biochemistry · 2024Review
- The Role of Pyroptosis in Coronary Heart Disease.Anatolian journal of cardiology · 2024Article
- Review
- The effect of macrophages and their exosomes in ischemic heart disease.Frontiers in immunology · 2024Review
- Mechanisms and therapeutic strategies of extracellular vesicles in cardiovascular diseases.MedComm · 2023Review
- Communications between macrophages and cardiomyocytes.Cell communication and signaling : CCS · 2023Review
- [LINC00926 promotes pyroptosis of hypoxia-induced human umbilical vein vascular endothelial cells by recruiting ELAVL1].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Exosomal Non-Coding RNA Mediates Macrophage Polarization: Roles in Cardiovascular Diseases.Biology · 2023Review
- Role of the N6-methyladenosine regulatory factor in reducing the risk of cardiovascular disease: subtype diagnosis following aerobic exercise-assisted weight loss.American journal of translational research · 2022Article
- Review
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The development of novel therapies targeting cardiomyocyte pyroptosis is needed for myocardial infarction (MI). The current study sought to analyze the role and mechanism of M2 macrophage-derived extracellular vesicles (M2-EVs) in cardiomyocyte pyroptosis after MI. M2 macrophages were induced, and M2-EVs were separated and characterized. A mouse model of MI was successfully established, followed by an assessment of myocardial injury and cardiomyocyte pyroptosis. An in vitro cell model was established, followed by a comprehensive evaluation of cell viability and pyroptosis. The binding relationships of miR-378a-3p and ELAVL1 [human antigen R (HuR)], HuR, and NLR family pyrin domain containing 3 (NLRP3) were analyzed. A functional rescue experiment was designed to validate the role of HuR. After M2-EV treatment, the cardiac functions of mice with MI were restored, the myocardial injury was attenuated and cardiomyocyte pyroptosis was reduced. In vitro, M2-EVs suppressed hypoxic cell injury and pyroptosis. Mechanistically, M2-EVs delivered miR-378a-3p into cardiomyocytes to upregulate miR-378a-3p expression and inhibit ELAVL1 (HuR) expression and transport of HuR to the cytoplasm, thus destabilizing NLRP3 and inhibiting activation of the NLRP3/Caspase-1/GSDMD pathways. Overexpression of HuR inhibited the protective effect of M2-EVs in cardiomyocytes. Overall, our findings showed that M2-EV-enveloped miR-378a-3p inhibited HuR expression and HuR translocation to the cytoplasm to destabilize NLRP3 and block activation of the NLRP3/Caspase-1/GSDMD pathways, thereby attenuating cardiomyocyte pyroptosis.
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