Abstract

The aim is to investigate the value and mechanism of action of LINC00963 in septic cardiomyopathy (SCM). A total of 85 patients with cardiomyopathy (control group) and 108 SCM patients were enrolled. An in vitro model was created by treating cardiomyocytes with 1 μg/mL of LPS. A sepsis mouse model was created using cecal ligation and puncture (CLP). Cox analysis was used to identify factors independently influencing mortality. Kaplan–Meier curves were used to record patient prognosis. RT-qPCR was used to detect gene expression. CCK8 and flow cytometry were employed to evaluate cell function. ELISA was used to detect inflammatory factor expression. Dual luciferase reporter and RIP validation were employed to confirm gene-targeted interactions. Upregulation of LINC00963 was observed in serum from patients with septic cardiomyopathy, heart tissue from septic mice, and LPS-infected cardiomyocytes, while miR-98-5p was downregulated. Patients with high LINC00963 expression had lower survival rates and were more likely to experience fatal outcomes. Both LINC00963 and BNP/NT-proBNP were both independent factors influencing patient mortality, and it was predicted that miR-98-5p was a target gene of LINC00963. Following si-LINC00963 transfection, apoptosis was reduced and inflammatory levels decreased in cardiomyocytes and myocardial tissue from sepsis-induced mice, and miR-98-5p was downregulated. However, the use of a miR-98-5p inhibitor reversed the cellular functional and inflammatory changes induced by LINC00963 knockdown. Knocking down LINC00963 reduces apoptosis and inflammation levels, and promotes cell proliferation by targeting miR-98-5p. This reduces the damage caused by sepsis to cardiomyocytes.