Exploring the autophagy-related pathogenesis of active ulcerative colitis

Area of Science:

• Molecular Biology
• Genomics
• Immunology

Background:

• Ulcerative colitis (UC) pathogenesis is complex, with current treatments offering incomplete relief.
• Understanding the molecular mechanisms of active UC is crucial for developing effective therapies.

Purpose of the Study:

• To investigate the role of autophagy in active ulcerative colitis (UC) pathogenesis using bioinformatics.
• To identify novel, autophagy-related therapeutic targets for UC.

Main Methods:

• Searched GEO database for UC datasets and identified differentially expressed genes (DEGs).
• Intersected DEGs with autophagy targets to find differentially expressed autophagy-related genes (DEARGs).
• Performed KEGG, GO, DisGeNET, and immune cell infiltration analyses; identified core targets using LASSO and PPI networks.

Main Results:

• Identified 58 DEARGs from 4822 DEGs; SERPINA1, BAG3, HSPA5, CASP1, and CX3CL1 emerged as core targets.
• DEARGs were enriched in autophagy regulation and macroautophagy pathways, and NOD-like receptor signaling.
• Found significant links between DEARGs and other diseases, and increased specific immune cells (CD4 T cells, follicular helper T cells) in active UC patients.

Conclusions:

• Autophagy plays a significant role in the active phase of ulcerative colitis.
• The identified core targets offer promising avenues for novel therapeutic strategies in active UC.