# Canonical pathways and selective mechanisms of autophagy in inflammatory bowel disease

## TL;DR

This review explores how autophagy, a cellular process, influences inflammatory bowel disease and identifies potential therapeutic targets.

## Contribution

The paper provides a systematic review of autophagy's role in IBD, emphasizing regulatory mechanisms and selective pathways.

## Key findings

- Dysregulation of autophagy components like ULK1 and Beclin 1 contributes to intestinal inflammation.
- Selective autophagy pathways such as mitophagy and xenophagy play context-dependent roles in IBD.
- Non-autophagic functions of autophagy-related genes may offer new therapeutic insights.

## Abstract

Inflammatory bowel disease (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder of the gastrointestinal tract. Autophagy, an essential intracellular homeostatic process, plays a pivotal role in the pathogenesis and progression of IBD. This review systematically examines recent advances in understanding the involvement of autophagy in IBD, with a particular focus on the regulatory mechanisms governing its sequential phases—initiation, elongation, and termination—and their respective contributions to intestinal inflammation. We highlight how dysregulation of core autophagy components, including the ULK1 complex, Beclin 1 complex, and ATG16L1, influences inflammatory responses. Furthermore, this article delves into the context-dependent roles of selective autophagy pathways such as mitophagy, ER-phagy, and xenophagy in IBD, as well as the emerging significance of non-autophagic functions exerted by autophagy-related genes. By integrating these multifaceted aspects, this review aims to provide a theoretical foundation and identify potential targets for future precision therapeutics targeting autophagy in IBD.