miR-892b targeting CTNNB1 regulates sepsis-induced myocardial dysfunction

Numerous sepsis patients experience myocardial damage, leading to a high mortality rate of sepsis. To investigate the clinical and functional role of miR-892b in sepsis-induced myocardial dysfunction (SMD). The expression of miR-892b and CTNNB1 in clinical subjects was measured by RT-qPCR, and their correlation was analyzed. An LPS-induced H9c2 cell damage model was established. CCK-8, cell apoptosis, and ELISA assays were utilized to assess cell viability, apoptosis, and levels of inflammatory cytokines. A dual-luciferase reporter assay was utilized to validate the target relationship. miR-892b is under-expressed in SMD patients, whilst CTNNB1 is overexpressed. The two show a negative correlation, and miR-892b displayed good diagnostic efficacy for SMD. LPS downregulates miR-892b in a dose- and time-dependent manner. Increasing miR-892b alleviates LPS-induced cellular damage, inhibits apoptosis, and the release of inflammatory mediators, and directly downregulates CTNNB1. Overexpression of CTNNB1 reverses the cardioprotective effects of miR-892b. miR-892b alleviates LPS-induced cardiomyocyte damage by inhibiting CTNNB1 expression and may serve as a potential diagnostic predictor and therapeutic target for SMD.