MiR-23b-3p ameliorates sepsis-induced acute lung injury by inhibiting SMAD3-mediated endothelial-mesenchymal transition.

ABSTRACT:

Background

Sepsis-associated acute lung injury (ALI) is driven by endothelial barrier dysfunction and endothelial-mesenchymal transition (EndoMT), mediated by TGF-β1/SMAD3 signaling. Despite the therapeutic potential of SMAD3, current inhibitors face limitations. As endogenous small molecules that are closely related to physiological regulatory processes, microRNAs (miRNAs) have more potential research value for regulating SMAD3. Therefore, this study aimed to investigate the protective effect and molecular mechanism of a key miRNA targeting SMAD3 in sepsis-ALI.

Methods

Screening multiple databases revealed that miR-23b-3p was the sole miRNA targeting SMAD3. Lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) and cecal ligation/puncture

SUBMITTER: Jiang L 

PROVIDER: S-EPMC12681251 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature