KDM6B promotes ferroptosis in rheumatoid arthritis fibroblast-like synoviocytes via the miR-128-3p/SLC7A11 axis through H3K27me3 modification.

ABSTRACT:

Background

Rheumatoid arthritis (RA) is a chronic inflammatory joint disease, primarily driven by fibroblast-like synoviocytes (FLSs) that trigger synovial inflammation and joint destruction. This study explores the mechanisms of KDM6B in ferroptosis in RA-FLSs, providing a theoretical basis for the treatment of RA.

Methods

RA-FLSs were isolated from RA synovial tissue samples. si-KDM6B was transfected into RA-FLSs, followed by the detection of KDM6B and miR-128-3p using qRT-PCR and Western blot. Cell viability was assessed using the CCK-8 assay. The levels of ROS, GSH, MDA, and Fe²⁺ were evaluated, and the expression of GPX4, SLC7A11, and ACSL4 was measured. The enrichment of KDM6B and H3K27me3 on the miR-128-3p promoter was detected by ChIP. The binding relation

SUBMITTER: Wang B 

PROVIDER: S-EPMC12482476 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature