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Our findings reveal that inflammatory macrophages deploy distinct, context-dependent redox-protective mechanisms to survive this self-inflicted stress, thereby avoiding ferroptotic cell death. Specifically, LPS-activated macrophages, M(LPS), rely on the GTP cyclohydrolase 1 (GCH1)\u2013tetrahydrobiopterin (BH4) pathway for ferroptosis resistance, whereas LPS\u2009+\u2009IFN-\u03b3\u2013activated macrophages, M(LPS\u2013IFN-\u03b3), depend primarily on nitric oxide produced by inducible nitric oxide synthase (iNOS)\u2014with the BH4 pathway suppressing cell death in the absence of nitric oxide. These distinct adaptations highlight a novel GCH1\u2013BH4\u2013iNOS axis that governs macrophage ferroptosis susceptibility. In both the LPS or the LPS\u2009+\u2009IFN-\u03b3\u2013activated settings, the redox-protective phenotype is reversible: Removal of inflammatory stimuli abolishes the protection, indicating that this metabolic programming requires continuous stimulation and is not a permanently fixed state. These findings uncover redox metabolism-guided metabolic distinctions between inflammatory macrophages and reveal how they preserve viability over prolonged inflammatory activation. Ultimately, our findings establish the GCH1\u2013BH4\u2013iNOS axis as a central, targetable mechanism to manipulate macrophage ferroptosis resistance for therapeutic purposes.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag146","type":"journal-article","created":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T00:04:02Z","timestamp":1781741042000},"source":"Crossref","is-referenced-by-count":2,"title":["Metabolic adaptations of inflammatory macrophages govern ferroptosis susceptibility via the GCH1\u2013BH4\u2013iNOS axis"],"prefix":"10.1093","volume":"215","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6784-5580","authenticated-orcid":false,"given":"Julia","family":"Sauer","sequence":"first","affiliation":[{"name":"Boehringer Ingelheim Pharma GmbH & Co. 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