Ischemic cardiovascular disease remains a leading cause of morbidity and mortality worldwide despite advances in pharmacological, interventional, and rehabilitative therapies. Hypoxia-inducible microRNA-210 (miR-210) has emerged as a central mediator of cellular adaptation to oxygen deprivation and ischemic injury. As a prototypical "hypoxamir," miR-210 regulates metabolic reprogramming, apoptosis, angiogenesis, and vascular remodeling, thereby influencing disease onset, progression, and repair. Its expression is governed by transcription factors, while downstream targets modulate mitochondrial function, DNA repair, and apoptotic signaling. Functionally, miR-210 enhances cardiomyocyte survival, promotes endothelial migration and tube formation, attenuates fibrosis, and supports stem cell adaptation. Clinical studies reveal that circulating and exosomal miR-210 correlate with infarct size, collateral formation, and prognosis, suggesting biomarker potential. Preclinical evidence further highlights therapeutic applications through mimics, antagomirs, nanoparticles, and stem cell-derived exosomes, though delivery and safety challenges remain. This review aims to synthesize current knowledge on the regulatory network and functional roles of miR-210 in ischemic cardiovascular disease, and to evaluate its prospects as both a biomarker and a therapeutic target.
Zhang et al. (Fri,) studied this question.