TRIM29 drives ulcerative colitis by disrupting lipid metabolism via lysosomal dysfunction: a multi-omics and experimental study.

ABSTRACT:

Background

The pathogenesis of ulcerative colitis (UC) involves genetic susceptibility and immune dysregulation. However, a more comprehensive understanding of its underlying mechanisms is still required.

Methods

Weighted correlation network analysis (WGCNA) and Mendelian randomization (MR) were used to investigate the association and causality between lipid metabolism and UC. Hub genes were identified by applying ensemble machine learning (LASSO, SVM, XGBoost) to the merged transcriptomic data, followed by cell-type-specific localization using public single-cell RNA-seq data from UC tissues. Pathophysiological relevance was confirmed in a DSS-induced colitis mouse model. The mechanistic role of the key hub gene was defined through knockdown LPS challenge in colonic epitheli

SUBMITTER: Guo XZ 

PROVIDER: S-EPMC12832330 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature