{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T05:08:27Z","timestamp":1789016907024,"version":"build-2803163510"},"reference-count":68,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T00:00:00Z","timestamp":1788307200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Antioxidants"],"abstract":"<jats:p>Retinitis pigmentosa (RP) is the most common inherited retinal dystrophy (prevalence ~1:4000) and a leading Mendelian cause of working-age blindness. Despite marked genetic heterogeneity, its progression converges on a common secondary cascade of outer-retinal hyperoxia, increased reactive oxygen species (ROS), and mitochondrial dysfunction that drives cone degeneration and central vision loss. Because this oxidative cascade is largely genotype-independent and pharmacologically tractable, oxidative stress is a cross-cutting therapeutic target. Within it, mitochondrial DNA (mtDNA) is a key element: once released from damaged photoreceptors\u2014free or within exosomes\u2014it may act as a damage-associated molecular pattern (DAMP), engaging TLR9, cGAS\u2013STING, and the NLRP3 inflammasome and sustaining chronic neuroinflammation. Extracellular mtDNA is therefore a potential integrative marker, simultaneously reflecting oxidative stress, mitochondrial dysfunction, cell death, and innate-immune activation. A central knowledge gap, however, remains: the mechanistic steps linking mtDNA to inflammation and to photoreceptor death have not been demonstrated in RP itself, and extracellular mtDNA has never been quantified in the ocular fluids of RP patients. In this review we appraise oxidative biomarkers in RP, propose extracellular mtDNA as a candidate biomarker of disease activity, and examine antioxidant and redox-modulating therapies\u2014from N-acetylcysteine and elamipretide trials to DAMP-sensor inhibition\u2014across experimental and clinical models. Finally, we propose extracellular mtDNA as a candidate pharmacodynamic endpoint and outline a path toward its validation.<\/jats:p>","DOI":"10.3390\/antiox15091110","type":"journal-article","created":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T14:35:29Z","timestamp":1788359729000},"page":"1110","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Oxidative\u2013Mitochondrial\u2013Inflammatory Axis in Retinitis Pigmentosa: Extracellular mtDNA as Biomarker and Therapeutic Read-Out"],"prefix":"10.3390","volume":"15","author":[{"given":"Rossella","family":"Grimaldi","sequence":"first","affiliation":[{"name":"Sense Organs Department, UOSD of Ophthalmology, Sapienza University of Rome, Polo Pontino-Ospedale A. Fiorini, 04019 Terracina, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-4685-5931","authenticated-orcid":false,"given":"Francesca","family":"Franco","sequence":"additional","affiliation":[{"name":"Sense Organs Department, UOSD of Ophthalmology, Sapienza University of Rome, Polo Pontino-Ospedale A. Fiorini, 04019 Terracina, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Enzo Maria","family":"Vingolo","sequence":"additional","affiliation":[{"name":"Sense Organs Department, UOSD of Ophthalmology, Sapienza University of Rome, Polo Pontino-Ospedale A. 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