FBLN1 regulates ferroptosis in acute respiratory distress syndrome by reducing free ferrous iron by inhibiting the TGF-β/Smad pathway.

ABSTRACT:

Background

Acute respiratory distress syndrome (ARDS) / acute lung injury (ALI) is a serious medical disease characterized by pulmonary dysfunction and inflammation. This study aims to determine the main molecular modules linked to ARDS and investigate the role of Fibulin-1 (FBLN1) in regulating ferroptosis in ARDS.

Methods

Weighted Gene Co-expression Network Analysis (WGCNA) was employed on the GSE263867 dataset to find key modules associated with ALI. Differentially expressed genes (DEGs) and protein-protein interaction (PPI) networks were analyzed. MLE-12 cells were treated with lipopolysaccharide (LPS) to induce ferroptosis. In vitro studies were conducted to investigate the effects of FBLN1 and Transforming Growth Factor Beta 1 (TGF-β) overexpression on cell viability,

SUBMITTER: Yuan Y 

PROVIDER: S-EPMC11643259 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature