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(cGAS-STING) pathway, a cornerstone of innate immunity, and ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, have traditionally been studied as distinct entities. However, emerging evidence reveals a complex and bidirectional crosstalk between these two pathways with profound implications for disease pathogenesis and therapy. This review systematically synthesizes the current understanding of the multifaceted interactions between the cGAS-STING pathway and ferroptosis. We detail the mechanisms by which STING signaling promotes ferroptosis through iron metabolism (e.g., NCOA4-mediated ferritinophagy), lipid peroxidation (e.g., via ACSL4 interaction), and GPX4 autophagic degradation. Conversely, we explore how ferroptosis, through mitochondrial DNA release and lipid peroxidation products, can activate the cGAS-STING pathway, amplifying immune and inflammatory responses. A novel, non-canonical role for mitochondrially-localized cGAS in suppressing ferroptosis independent of STING is also highlighted, adding a layer of complexity to this interplay. We consolidate evidence of this crosstalk across a spectrum of diseases, including cancer, infectious diseases, neurodegenerative disorders, and ischemia-reperfusion injuries. In cancer, leveraging this interplay\u2014particularly by inducing ferroptosis to activate STING-dependent anti-tumor immunity\u2014presents promising therapeutic strategies. In contrast, for inflammatory and organ injuries, concurrent inhibition of both pathways may mitigate damage. This review underscores the STING-ferroptosis axis as a critical regulatory node and a promising frontier for developing novel therapeutic interventions across diverse human diseases.<\/jats:p>","DOI":"10.1038\/s41420-026-03214-8","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T23:49:37Z","timestamp":1783381777000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The emerging Nexus of STING signaling and ferroptosis: from mechanisms to therapeutic opportunities"],"prefix":"10.1038","volume":"12","author":[{"given":"Xixi","family":"Lin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yihong","family":"Wen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiaheng","family":"Lang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziyu","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zijie","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0526-1990","authenticated-orcid":false,"given":"Linbo","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0710-0739","authenticated-orcid":false,"given":"Feiyang","family":"Ji","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-9023-2495","authenticated-orcid":false,"given":"Lili","family":"Zhi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0727-4034","authenticated-orcid":false,"given":"Jichun","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,7,7]]},"reference":[{"key":"3214_CR1","doi-asserted-by":"publisher","first-page":"1060","DOI":"10.1016\/j.cell.2012.03.042","volume":"149","author":"SJ Dixon","year":"2012","unstructured":"Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. 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