# Epigenetic Landscapes in Ulcerative Colitis: From Mechanistic Insights to Clinical Translation

## TL;DR

This review explores how epigenetic changes contribute to ulcerative colitis and highlights their potential for new treatments.

## Contribution

The paper synthesizes current research on epigenetic mechanisms in UC, focusing on DNA methylation, histone modification, and noncoding RNAs.

## Key findings

- Epigenetic modifications influence intestinal and inflammatory cell behaviors in UC.
- DNA methylation, histone modification, and ncRNAs are key players in UC pathogenesis.
- Epigenetics offers potential for new diagnostic and therapeutic targets in UC.

## Abstract

Ulcerative colitis (UC) is distinguished by nonspecific
inflammation
and ulceration of the rectal and colonic mucosa. The conventional
therapeutic modalities for UC exhibit restricted efficacy, underscoring
the importance of advancing novel mechanisms and therapeutic interventions.
The field of epigenetics, encompassing DNA methylation, histone modification,
noncoding RNAs (ncRNAs), and RNA modification, is progressively illuminating
the association with UC. Moreover, the current focus of intense scrutiny
in drug development is the utilization of epigenetics as a potential
target for anti-UC therapy. Significantly, the aberrant epigenetic
modifications exert influence over various behaviors exhibited by
intestinal epithelial cells and inflammatory cells. In this review,
we have examined and synthesized current clinical and experimental
research to comprehensively analyze the expression patterns and elucidate
the underlying mechanisms of epigenetic alterations in the advancement
of UC, with a particular focus on DNA methylation, histone modification,
ncRNAs (miRNA, lncRNA, and circRNA), and RNA modification. Additionally,
we discussed the obstacles and the potential future directions related
to epigenetic modifications in UC. Deciphering the intricate epigenetic
modifications in UC offers potential for yielding novel understandings
of the disease’s etiology and pathogenesis and the identification
of diagnostic and therapeutic targets, thereby establishing a basis
for achieving optimal outcomes in UC.