FXR acts as a therapeutic target for ulcerative colitis via suppressing ferroptosis.

ABSTRACT:

Background

The involvement of ferroptosis in ulcerative colitis (UC) is increasingly acknowledged. Several investigations have revealed the various mechanisms by which the farnesoid X receptor (FXR) inhibits ferroptosis in certain diseases; however, its potential modulation of ferroptosis in UC remains unexplored.

Methods

The characteristics of FXR expression in colitis were evaluated in the GEO database, patient specimens, and mice with DSS-induced colitis. The role of FXR in ferroptosis was investigated by treating colitis mice with the intestine-restricted FXR agonist fexaramine (Fex) intragastrically. In vitro, Caco-2 cells challenged with RSL3 were used to study the role of FXR in modulating ferroptosis in intestinal epithelial cells (IECs).

Results

Fex significa

SUBMITTER: Zhao C 

PROVIDER: S-EPMC12273381 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature