{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T01:42:57Z","timestamp":1791855777674,"version":"4.3.4"},"reference-count":328,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T00:00:00Z","timestamp":1786579200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Mitochondrial DNA (mtDNA) is increasingly recognized as an active driver of immune dysregulation in systemic lupus erythematosus (SLE), yet most existing reviews treat it as a single damage signal rather than a multifunctional pathological mediator. This review presents an integrated framework examining mtDNA as a central hub linking mitochondrial dysfunction to systemic autoimmunity. We conducted a comprehensive synthesis of published evidence on mtDNA biology, its dysregulation in SLE, organ-specific injury mechanisms, and the clinical landscape of mtDNA-targeted therapeutic strategies. In SLE, intracellular mtDNA depletion coexists paradoxically with markedly elevated circulating cell-free mtDNA, a pattern correlating with disease activity and organ involvement. Sequential cytoplasmic and extracellular release of mtDNA engages cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING), Toll-like receptor 9 (TLR9), and inflammasome platforms, establishing self-amplifying interferon and pro-inflammatory circuits that drive multi-organ pathology. We consolidate emerging evidence for mtDNA-related parameters as clinical biomarkers and propose a provisional patient stratification framework distinguishing two pathological subtypes with distinct therapeutic implications. Among current therapeutic strategies, N-acetylcysteine (NAC) and metformin carry the strongest clinical evidence, while cGAS-STING inhibitors and TLR9 antagonists represent compelling emerging candidates. mtDNA operates as an integrative pathological hub in SLE, and its dysregulation pattern carries both diagnostic and therapeutic significance. Incorporating mtDNA-based biomarkers into clinical monitoring and developing precision strategies targeting mtDNA-driven inflammatory circuits represent important steps toward individualized SLE management.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1928003","type":"journal-article","created":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T12:57:35Z","timestamp":1786625855000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies"],"prefix":"10.3389","volume":"17","author":[{"given":"Fugang","family":"Huang","sequence":"first","affiliation":[{"name":"The First School of Clinical Medicine, Zhejiang Chinese Medical University","place":["Hangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ke","family":"Sun","sequence":"additional","affiliation":[{"name":"The Third 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