Diab Vasc Dis Res. 2026 Jul-Aug;23(4):14791641261454501. doi: 10.1177/14791641261454501. Epub 2026 Jul 22.
ABSTRACT
ObjectiveThis work aimed to verify the value of miR-143-3p in diabetic cardiomyopathy (DCM).MethodsThe ROC curve, correlation analysis, and multivariate Logistic regression analysis assessed the diagnostic value, association with DCM, and DCM risk factors. Bioinformatic analysis predicted the downstream targets of miR-143-3p. Dula-luciferase reporter assay validated the interaction between miR-143-3p and ERBB3. In vitro high glucose (HG)-stimulated cardiomyocyte (AC16) injury was employed to clarify the mechanism of the miR-143-3p/ERBB3 axis in DCM.ResultsUpregulation of miR-143-3p was observed in the DM group and further elevated in the DCM group compared with healthy individuals. The upregulated miR-143-3p expression distinguished subjects with DM from healthy individuals and diagnosed subjects with DCM from DM. MiR-143-3p expression was associated with blood glucose, myocardial injury, and cardiac function of DCM, and predicted the risk for DCM development. In vitro, the inhibition of miR-143-3p attenuated HG-induced AC16 cell injury through improving cell proliferation, suppressing apoptosis, inflammation, oxidative stress, and the release of myocardial enzymes by upregulating the ERBB3 expression.ConclusionsUpregulation of miR-143-3p showed a diagnostic potential for DCM and predicted the progression of DCM. In vitro, miR-143-3p promoted HG-induced cardiomyocyte injury by targeting ERBB3, which might provide novel insights for DCM clinical management.
PMID:42484618 | DOI:10.1177/14791641261454501