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These defects impair energy production, increases oxidative stress, and disrupts immune balance. Here we review three therapeutic classes that target mitochondrial pathways: antioxidants, metabolic modulators, and microbiota\u2010directed strategies. In UC, mitochondrial dysfunction creates a self\u2010perpetuating cycle through metabolic\u2010immune crosstalk, the leakage of mitochondrial DNA, and the redistribution of cardiolipin. Moreover, the gut microbiota and mitochondria engage in bidirectional crosstalk that amplifies intestinal inflammation. Encouragingly, agents that restore mitochondrial function have shown therapeutic benefit in preclinical and early clinical studies. Notable examples include the mitochondria\u2010targeted antioxidant MitoQ (currently in a Phase 2b trial for UC), ClpP (caseinolytic protease P) activators that reprogram T\u2010cell metabolism, and engineered probiotics that deplete pro\u2010inflammatory succinate. This review synthesizes current evidence on mitochondrial dysfunction in UC, bridging molecular mechanisms, immune\u2010metabolic interactions, and emerging therapeutics to propose a new treatment paradigm centered on mitochondrial restoration.<\/jats:p>","DOI":"10.1002\/jbt.71021","type":"journal-article","created":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T18:09:07Z","timestamp":1784138947000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Mitochondrial Dysfunction in Ulcerative Colitis: Pathogenic Mechanisms and Novel Therapeutics"],"prefix":"10.1002","volume":"40","author":[{"given":"Hongyan","family":"Ran","sequence":"first","affiliation":[{"name":"College of Pharmacy and Bioengineering Chongqing University of Technology Chongqing People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siyuan","family":"Zhou","sequence":"additional","affiliation":[{"name":"College 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