Circulating miR-106b-5p discriminates acute myocardial infarction patients, predicts disease severity, and regulates H/R-induced cardiomyocyte injury by targeting CDKN1A

The early detection, disease monitoring, and prognosis prediction are of great significance for acute myocardial infarction (AMI). This study focused on miR-106b-5p, evaluating its clinical significance in AMI onset and progression. This study enrolled 147 AMI patients with 123 stable angina pectoris (SAP) patients as the control group. The serum miR-106b-5p was compared between the two groups, and its diagnostic potential was evaluated. The involvement of miR-106b-5p in AMI severity was assessed based on its association with patients’ cardiac function and disease conditions. In vitro, hypoxia/reoxygenation (H/R) cell modeling was established with H9C2 cells. The regulatory effect of miR-106b-5p on cell viability, apoptosis, oxidative stress, and mitochondrial function was evaluated. The involvement of CDKN1A in the function of miR-106b-5p was estimated to elucidate the regulatory mechanisms. Significant upregulation of miR-106b-5p was observed in AMI patients, which significantly discriminated AMI patients. Increasing serum miR-106b-5p was positively correlated with Killip grade and the number of lesion branches in AMI patients. For the cardiac function, miR-106b-5p showed a negative correlation with LVEF and positive correlations with E/A ratio, LVEDV, and LVESV in AMI patients. Patients with higher serum miR-106b-5p levels showed a high incidence rate of recurrence. The knockdown of miR-106b-5p alleviated H/R-induced reduction in cell viability, increasing cell apoptosis, enhancing oxidative stress, and suppressing mitochondrial dysfunction. Silencing CDKN1A could reverse the regulatory effect of miR-106a-5p on H/R-induced cardiomyocyte injury. miR-106b-5p discriminated AMI patients, indicated disease severity, and predicted patients’ prognosis. Silencing miR-106b-5p alleviated H/R-induced cardiomyocyte injury by targeting CDKN1A.