Key result
N-EVs delivering miR-16-5p reduce myocardial injury in AMI by suppressing CYP1B1-mediated PANoptosis.
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Why the study?
Do circulating extracellular vesicles from healthy controls mitigate myocardial injury and PANoptosis in ischemia-reperfusion models?
Do circulating extracellular vesicles from healthy controls mitigate myocardial injury and PANoptosis in ischemia-reperfusion models?
Circulating extracellular vesicles from healthy individuals protect against myocardial ischemia-reperfusion injury by delivering miR-16-5p to suppress PANoptosis, suggesting a potential therapeutic strategy for acute myocardial infarction.
BACKGROUND: Acute myocardial infarction (AMI) is a leading global cause of death, with extracellular vesicles (EVs) emerging as potential therapeutic mediators. However, the mechanisms by which circulating EVs from different sources influence myocardial injury remain unclear. METHOD: Circulating EVs from AMI patients (AMI-EVs) and healthy controls (N-EVs) were isolated. In vitro assays (CCK8, EdU, flow cytometry, wound healing, angiogenesis) evaluated their effects on cardiomyocyte/endothelial cell proliferation, apoptosis, migration, and tube formation. Immune cell infiltration and immunoglobulin levels in myocardial injury patients were analyzed. Microarray and qPCR identified differentially expressed miRNAs in EVs. CYP1B1, predicted as a target of miR-16-5p via bioinformatics, was validated using dual-luciferase reporter and RNA co-immunoprecipitation. An ischemia-reperfusion (I/R) mouse model assessed EV effects on myocardial injury and PANoptosis. RESULT: N-EVs alleviated I/R-induced myocardial injury in vivo and protected cardiomyocytes/endothelial cells from H2O2-induced damage in vitro. Patients with myocardial injury exhibited IgG deposits, immune cell infiltration, and elevated IgG1/IgG3 levels. N-EVs promoted angiogenesis and cardiomyocyte proliferation while suppressing PANoptosis (combined apoptosis, necroptosis, pyroptosis). Mechanistically, miR-16-5p was enriched in N-EVs and directly targeted CYP1B1, inhibiting its expression and downstream PANoptosis pathways. CONCLUSION: N-EVs mitigate myocardial injury by delivering miR-16-5p to suppress CYP1B1-mediated PANoptosis, highlighting their role in intercellular communication and therapeutic potential for AMI. This study provides insights into EV-based strategies for cardiac repair and fibrosis prevention.
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Zhang et al. (2026) studied Acute myocardial infarction. Circulating EVs from healthy controls (N-EVs) vs. Circulating EVs from AMI patients (AMI-EVs) / Control was evaluated on Myocardial injury and PANoptosis. Circulating EVs from healthy controls mitigated myocardial injury and suppressed CYP1B1-mediated PANoptosis by delivering miR-16-5p in vitro and in an ischemia-reperfusion mouse model.
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