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Increased TH levels in circulation are associated with a higher incidence of age-related macular degeneration. In mice, TH treatment causes photoreceptor degeneration, which is accompanied by an increase in receptor-interacting serine\/threonine-protein kinase 3 (RIPK3) in the retina. Here, we investigated the contribution of RIPK3\/necroptosis to TH-induced photoreceptor degeneration using mice deficient in RIPK3 and the necroptotic mixed lineage kinase domain-like protein (MLKL). Wild-type (C57BL\/6) and mutant mice at postnatal day 30 received triiodothyronine (T3, 20 \u00b5g\/mL in drinking water) for four weeks, followed by the evaluation of photoreceptor survival\/death and retinal function. Deletion of Ripk3 preserved photoreceptor integrity against T3-induced degeneration, evidenced by improved retinal morphology, increased cone density, improved retinal light responses, and reduced cell death. This protection was observed in both global and photoreceptor-specific Ripk3 knockout mice. In contrast, the deletion of Mlkl did not protect photoreceptors. This work supports the view that RIPK3, but not MLKL, contributes to TH-induced photoreceptor degeneration. The lack of protection from Mlkl deletion suggests that RIPK3\u2019s action is likely mediated via a necrosome-independent mechanism. These findings provide significant insight into how TH signaling induces photoreceptor degeneration and implicate RIPK3 as a potential therapeutic target.<\/jats:p>","DOI":"10.3390\/ijms26178154","type":"journal-article","created":{"date-parts":[[2025,8,22]],"date-time":"2025-08-22T12:31:26Z","timestamp":1755865886000},"page":"8154","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["RIPK3 Contributes to Thyroid Hormone-Induced Photoreceptor Degeneration"],"prefix":"10.3390","volume":"26","author":[{"given":"Lilliana R.","family":"York","sequence":"first","affiliation":[{"name":"Department of Cell Biology, University of Oklahoma Health Sciences, Oklahoma City, OK 73104, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hongwei","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Oklahoma Health Sciences, Oklahoma City, OK 73104, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yun","family":"Le","sequence":"additional","affiliation":[{"name":"Departments of Medicine Endocrinology, Cell Biology, and Ophthalmology, and Harold Hamm Diabetes Center, University of Oklahoma Health Sciences, Oklahoma City, OK 73104, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Courtney T.","family":"Griffin","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Oklahoma Health Sciences, Oklahoma City, OK 73104, USA"},{"name":"Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xi-Qin","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, University of Oklahoma Health Sciences, Oklahoma City, OK 73104, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2025,8,22]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"457","DOI":"10.1002\/jcp.20346","article-title":"Oxidative damage is a potential cause of cone cell death in retinitis pigmentosa","volume":"203","author":"Shen","year":"2005","journal-title":"J. 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