The regulatory role of post-translational modifications in the pathogenesis of ulcerative colitis

Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease characterized by mucosal inflammation limited to the colon, which may progress to pancolitis in severe cases. This debilitating condition significantly impairs patients' quality of life and may result in long-term disability, representing a growing global public health concern. Despite extensive research, the precise pathogenesis of UC remains incompletely understood. Current evidence implicates a multifactorial etiology involving genetic susceptibility, immune dysregulation, intestinal barrier dysfunction, and gut microbiota imbalance. Protein post-translational modifications (PTMs), including phosphorylation, glycosylation, acetylation, methylation, ubiquitination, citrullination, and palmitoylation, have emerged as key regulatory mechanisms in cellular biology. These modifications play pivotal roles in modulating protein activity, structural stability, protein-protein interactions, and intracellular signaling pathways. Furthermore, PTMs are involved in immune regulation and the maintenance of cellular homeostasis. This review provides a comprehensive overview of the roles and mechanisms of various PTMs in UC pathogenesis, with an emphasis on their involvement in regulating immune function, epithelial integrity, and inflammatory signaling. Elucidating the contribution of PTMs to UC may offer novel insights into disease mechanisms and provide promising therapeutic targets for future treatment strategies.