ArticleFrontiers in physiology2026
MiR-200a-3p protects against myocardial ischemia-reperfusion injury via KEAP1-NRF2 signaling.
Article in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Abstract
Background: Myocardial ischemia/reperfusion (I/R) injury is a major challenge in reperfusion therapy for acute myocardial infarction, primarily due to excessive oxidative stress, inflammation, and cardiomyocyte apoptosis. MicroRNAs are known regulators of cellular stress responses, but the role and underlying mechanism of miR-200a-3p in myocardial I/R injury remain unclear. Methods: Results: MiR-200a-3p was markedly downregulated in H/R-treated cardiomyocytes and in mouse hearts after I/R injury. Restoring miR-200a-3p enhanced cell viability, reduced apoptosis, ROS accumulation, lipid peroxidation, and inflammatory cytokine release, and restored antioxidant defenses Conclusion: These findings indicate that miR-200a-3p protects against myocardial I/R injury by targeting KEAP1 and activating NRF2-dependent antioxidant signaling, identifying a novel redox-regulatory axis with therapeutic potential, with beneficial effects on myocardial injury and its associated functional impairment.
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