ArticleStem cell research & therapy2025
Exosomal miR-202-5p derived from iPSC-MSCs protects against myocardial infarction through inhibition of cardiomyocyte pyroptosis.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Stem Cell-Derived Mitochondria-Enriched Preservation Solutions as Organelle-Based Therapeutic Strategy for Cold Storage of Liver and Kidney.Advanced healthcare materials · 2026Article
- P2X7-NEK7-NLRP3 Axis Drives Cardiac Inflammation and Fibrosis in Isoproterenol-Induced Cardiac Remodeling in Mice.Acta physiologica (Oxford, England) · 2026Article
- Mesenchymal Stem Cell-Derived Exosomes: A Tool for Heart Failure Repair - From Molecular Mechanisms to Clinical Potential.Journal of inflammation research · 2026Review
- Extracellular Vesicles in the Heart-Organ Axis: From Inter-Organ Communication to Precision Nanomedicine for Heart Diseases.International journal of nanomedicine · 2026Review
- NLRP3-mediated pyroptosis in cardiovascular disease: from molecular mechanisms to therapeutic targets.Frontiers in pharmacology · 2026Review
- Mitochondria-Enriched Extracellular Vesicles (EVs) for Cardiac Bioenergetics Restoration: A Scoping Review of Preclinical Mechanisms and Source-Specific Strategies.International journal of molecular sciences · 2025Article
- Mesenchymal Stem Cell-Derived Exosomes in Anti-NET Therapy: Mechanisms, Challenges, and Future Perspectives.International journal of nanomedicine · 2025Review
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
backgroundNOD-like receptor thermal protein domain associated protein 3 (NLRP3)-mediated pyroptosis of cardiomyocytes is a key contributor to the progression of myocardial infarction (MI). This study aimed to investigate whether exosomes derived from human induced pluripotent stem cell-derived mesenchymal stem cells (iPSC-MSC-EXOs) could protect against MI by inhibiting cardiomyocyte pyroptosis and explore the underlying mechanisms.
methodsExosomes from human bone marrow-MSCs (BM-MSC-EXOs) and iPSC-MSCs (iPSC-MSC-EXOs) were collected and intramuscularly injected into the peri-infarct region of a mouse MI model. Cardiac function was assessed four weeks post-injection. Myocardial pyroptosis was evaluated using TUNEL staining and measurement of associated factors. Neonatal mouse cardiomyocytes (NMCMs) exposed to serum deprivation and hypoxia (SD/H) were treated with BM-MSC-EXOs or iPSC-MSC-EXOs. A loss-of-function approach was employed to examine the role of iPSC-MSC-exosomal-miR-202-5p in regulating cardiomyocyte pyroptosis.
resultsCompared to BM-MSC-EXOs, iPSC-MSC-EXOs demonstrated superior improvement in cardiac function in MI mice. Both BM-MSC-EXOs and iPSC-MSC-EXOs reduced cardiomyocyte pyroptosis by downregulating proteins NLRP3, ASC, Caspase-1, and gasdermin D-NT, as well as inflammatory factors in MI mice and SD/H-treated NMCMs. iPSC-MSC-EXOs exhibited greater protective effects. MicroRNA sequencing revealed higher levels of miR-202-5p in iPSC-MSC-EXOs than in BM-MSC-EXOs. The protective effect of iPSC-MSC-EXOs against cardiomyocyte pyroptosis was partially reversed by miR-202-5p knockdown. Mechanistically, miR-202-5p in iPSC-MSC-EXOs inhibited cardiomyocyte pyroptosis by downregulating the TRAF3IP2/JNK pathway.
conclusionsiPSC-MSC-EXOs protect against MI by inhibiting cardiomyocyte pyroptosis via miR-202-5p-mediated suppression of the TRAF3IP2/JNK axis. These findings suggest a promising therapeutic approach for MI.
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