ArticleBMC medicine2026
Targeting cardiomyocyte-derived extracellular vesicle miR-574-5p protects against cognitive impairment induced by ischemia-reperfusion.
Article in BMC medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Small extracellular vesicles induced by Angiotensin-(1-7) enhance cardioprotection following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2026Article
- Exosome-Mediated Systemic Signaling: Mechanisms, Disease Integration, and Translational Potential.Current issues in molecular biology · 2026Review
- Bidirectional brain-heart communication in coronary heart disease: from coronary plaques to central autonomic networks.Frontiers in neuroscience · 2026Review
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Authors and funding
14 authors.
Funding
Abstract
backgroundAcute myocardial ischemia/reperfusion (MI/R) increases risk for cognitive decline, yet the underlying mechanisms mediating heart-brain communication remain poorly understood. Small extracellular vesicles (sEVs) have emerged as novel long-range signaling mediators and may play a critical role.
methodsMI/R was induced by transient ligation of the left anterior descending artery. Cognitive performance was assessed using multiple behavioral tests. sEVs derived from cardiomyocytes were labeled to track their distribution and cellular uptake in the brain. Heart and brain tissues were analyzed for microRNAs (miRNAs) expression using bioinformatics, qPCR, and RNAScope. The role of specific miRNAs was investigated through genetic inhibition of cardiomyocyte-derived sEVs release using Rab27a
resultsMI/R mice exhibited significant cognition deficits along with hypothalamic paraventricular nucleus (PVN) synaptic ultrastructural injury and dysfunction. sEVs released from injured cardiomyocytes were significantly elevated and preferentially accumulated in oxytocin neurons from the PVN. Inhibiting cardiomyocyte-derived sEVs ameliorated cognitive impairments and synaptic pathology. Conversely, injection of cardiomyocyte-derived sEVs into the PVN recapitulated MI/R-induced cognitive deficits. Among candidate miRNAs, miR-574-5p was identified as a key mediator. Its inhibition via miRNA sponge restored cognitive function. Bioinformatic analyses revealed that miR-574-5p targets genes involved in synaptic structure and GABA
conclusionsCardiomyocyte-derived sEVs contribute to MI/R-induced cognitive impairment through miR-574-5p. Upon delivery to the PVN and uptake by oxytocin neurons, miR-574-5p suppresses synaptic and GABA
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Registered trials
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