MiR-361-3p overexpression promotes apoptosis and inflammation by regulating the USP49/IκBα/NF-κB pathway to aggravate sepsis-induced myocardial injury.

ABSTRACT:

Background

Sepsis is a major cause of in-hospital death, particularly in the intensive care unit. A huge amount of effort has been put into identifying reliable biomarkers to improve the prognosis of patients with sepsis. Among the numerous candidates, microRNAs have attracted attention because of their promising prognostic value. Multiple miRNAs have been suggested to play vital roles in manipulating the nuclear factor-kappa B (NF-κB) pathway, a key factor involved in sepsis. In this study, we attempted to elucidate the potential functions of miR-361-3p in sepsis-induced myocardial injury in vivo and in vitro.

Methods

A sepsis model was established by cecal ligation and puncture (CLP) in rats and by lipopolysaccharide (LPS) in H9c2 cells. The functions of miR-361-3p were re

SUBMITTER: Geng H 

PROVIDER: S-EPMC11574052 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature