ArticleFrontiers in cell and developmental biology2026
Circulating exosomal miR-550a-5p/miR-665 identify coronary microvascular dysfunction and drive endothelial-myocyte crosstalk in type 2 diabetes.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Recent Advances in Comprehending Endothelial Dysfunction and Diabetic Cardiomyopathy: From Molecular Mechanisms to Clinical Applications.Journal of cardiovascular development and disease · 2026Review
- Extracellular Vesicles as Mediators of Pathophysiology and Disease Progression in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Extracellular Vesicle-Derived MicroRNAs as Early Diagnostic Biomarkers of Diabetic Nephropathy and Cardiovascular Diseases in Type 2 Diabetes.International journal of molecular sciences · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
Objective: This study aimed to identify circulating exosomal microRNAs for early detection of coronary microvascular dysfunction (MD) and stratification of myocardial injury risk in type 2 diabetes, and to test whether miR-550a-5p derived from endothelial cell models mechanistically links endothelial stress to cardiomyocyte vulnerability via Hippo-eNOS signaling and vesicular transfer. Method: We combined Gene Expression Omnibus (GEO)-guided discovery and compendium prioritization with clinical and mechanistic validation. Plasma exosomal miR-550a-5p/miR-665 were quantified in a well-phenotyped Type 2 Diabetes Mellitus (T2DM) cohort and related to MD and myocardial injury. Result: Exosomal miR-550a-5p and miR-665 were elevated in MD and further increased with myocardial injury, showing useful diagnostic performance and independent associations. miR-550a-5p inhibition restored endothelial viability, migration, tube formation and p-eNOS/eNOS, reduced MST1/LATS1 activation, and increased Yes-associated protein (YAP) activity. Endothelial exosomes delivered miR-550a-5p to cardiomyocytes, aggravating apoptosis and oxidative stress; donor-cell miR-550a-5p suppression and Hippo inhibition mitigated these effects. Conclusion: Exosomal miR-550a-5p, together with miR-665, functions as a dual-utility signal, serving as an accessible biomarker for coronary MD and as a mechanistic mediator in endothelial-to-cardiomyocyte exosomal signaling. These findings support earlier detection, risk stratification, and mechanism-guided intervention in T2DM. Future priorities include external validation, longitudinal kinetic assessment, and target-network mapping.
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