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Inflammatory bowel disease (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder of the gastrointestinal tract driven by complex interactions among genetic susceptibility, barrier dysfunction, and immune dysregulation. Mitophagy, the selective autophagic clearance of damaged mitochondria, has emerged as a key regulator of intestinal homeostasis and immune balance. Impaired mitophagy compromises epithelial barrier integrity, amplifies inflammatory signaling, and promotes disease progression. This review summarizes the molecular mechanisms of mitophagy, examines its involvement in IBD pathogenesis across intestinal epithelial and immune cell compartments, and highlights mitophagy-modulating compounds that may inform the development of novel therapeutic strategies.
Chen et al. (Thu,) studied this question.