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The seemingly distinct pathologies exhibit shared microenvironmental hallmarks\u2014oxidative stress, immune dysregulation, and metabolic reprogramming\u2014that converge on ferroptosis regulation. This review synthesizes how ferroptosis operates at the intersection of these diseases, acting as both a tumor\u2010suppressive mechanism and a driver of inflammatory tissue damage. In cancer, ferroptosis eliminates therapy\u2010resistant cells but paradoxically facilitates metastasis through lipid peroxidation byproducts that remodel the tumor microenvironment and suppress antitumor immunity. In chronic inflammatory diseases\u2014from atherosclerosis to rheumatoid arthritis\u2014ferroptosis amplifies neuroinflammatory cascades while simultaneously exposing vulnerabilities for therapeutic targeting. Central to this duality are shared regulatory nodes, including nuclear factor kappa B\u2010driven inflammation, NOD\u2010like receptor family pyrin domain\u2010containing 3 inflammasome activation, and GPX4 dysfunction. Therapeutically, ferroptosis induction shows promise against therapy\u2010resistant cancers but risks exacerbating inflammatory damage, underscoring the need for precision modulation. Emerging strategies\u2014nanoparticle\u2010based inducers, immunotherapy combinations, and biomarker\u2010guided patient stratification\u2014aim to balance prodeath efficacy against off\u2010target toxicity. By dissecting the ferroptosis\u2013inflammation\u2013cancer axis, this review provides a unified framework for understanding disease pathogenesis and advancing therapies for conditions resistant to conventional treatments. Future research must prioritize spatial mapping of ferroptosis dynamics, mechanistic crosstalk with immune checkpoints, and combinatorial regimens that exploit ferroptosis vulnerabilities while mitigating its inflammatory consequences.<\/jats:p>","DOI":"10.1002\/mco2.70349","type":"journal-article","created":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T06:43:08Z","timestamp":1756968188000},"source":"Crossref","is-referenced-by-count":38,"title":["Ferroptosis in Cancer and Inflammatory Diseases: Mechanisms and Therapeutic Implications"],"prefix":"10.1002","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-1754-6428","authenticated-orcid":false,"given":"Guangyi","family":"Shen","sequence":"first","affiliation":[{"name":"Department of Urology The Second Xiangya Hospital Central South University  Changsha Hunan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiachen","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of 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Key Laboratory of Diabetes Immunology (Central South University) Ministry of Education  Changsha China"},{"name":"Department of Nephrology The Second Xiangya Hospital Central South University  Changsha Hunan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fei","family":"Deng","sequence":"additional","affiliation":[{"name":"Department of Urology The Second Xiangya Hospital Central South University  Changsha Hunan China"},{"name":"National Clinical Research Center for Metabolic Disease Key Laboratory of Diabetes Immunology (Central South University) Ministry of Education  Changsha China"},{"name":"Department of Nephrology The Second Xiangya Hospital Central South University  Changsha Hunan 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