{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T07:07:37Z","timestamp":1789542457172,"version":"build-2803163510"},"reference-count":96,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"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. Cell Dev. Biol."],"abstract":"<jats:p>The eye is one of the most metabolically active organs, and mitochondria serve as the central hub for cellular energy metabolism by providing adenosine triphosphate through oxidative phosphorylation. Disruption of mitochondrial metabolism\u2014including insufficient adenosine triphosphate synthesis, excessive production of reactive oxygen species, and dysregulated quality control\u2014can trigger various ocular diseases. Common blinding diseases such as myopia, diabetic retinopathy, and glaucoma are closely associated with mitochondrial dysfunction in specific cell types. This review delineates the mechanisms by which metabolic adaptations in scleral fibroblasts induce myopia and the synergistic action of lipofuscin, the high-glucose-triggered mitochondrial reactive oxygen species bursts and metabolic memory in diabetic retinopathy, and the roles of mitochondrial dynamics imbalance and energy exhaustion in trabecular meshwork cells in glaucoma. Based on these mechanisms, the article proposes intervention strategies targeting mitochondrial antioxidant defense, enhancing mitochondrial biogenesis, regulating mitochondrial dynamics, and restoring mitophagy, aiming for precise prevention and treatment of ocular diseases at the mitochondrial level.<\/jats:p>","DOI":"10.3389\/fcell.2026.1961856","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T06:57:19Z","timestamp":1789541839000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The key mechanisms and intervention strategies of cell-type-specific mitochondrial metabolism in ophthalmic diseases"],"prefix":"10.3389","volume":"14","author":[{"given":"Shouyao","family":"Zhang","sequence":"first","affiliation":[{"name":"Yunnan University of Chinese Medicine, The First Clinical Medical School","place":["Kunming, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaochun","family":"Yang","sequence":"additional","affiliation":[{"name":"The First People\u2019s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Department of Ophthalmology","place":["Kunming, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenggui","family":"Xu","sequence":"additional","affiliation":[{"name":"Yunnan University of Chinese Medicine, The Second Clinical Medical School","place":["Kunming, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuang","family":"Wang","sequence":"additional","affiliation":[{"name":"Yunnan University of Chinese Medicine, The Second Clinical Medical School","place":["Kunming, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiantao","family":"Tai","sequence":"additional","affiliation":[{"name":"Yunnan University of Chinese Medicine, The Second Clinical Medical School","place":["Kunming, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,16]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1066","DOI":"10.1016\/j.bbadis.2016.11.010","article-title":"Mitochondrial dysfunction and oxidative stress in metabolic disorders - a step towards mitochondria based therapeutic strategies","volume":"1863","author":"Bhatti","year":"2017","journal-title":"Biochimica biophysica acta Mol. basis Dis."},{"key":"B2","doi-asserted-by":"publisher","first-page":"101201","DOI":"10.1016\/j.redox.2019.101201","article-title":"Mitochondrial oxidative stress in the retinal pigment epithelium (RPE) led to metabolic dysfunction in both the RPE and retinal photoreceptors","volume":"24","author":"Brown","year":"2019","journal-title":"Redox Biology"},{"key":"B3","doi-asserted-by":"publisher","first-page":"13585","DOI":"10.1038\/s41598-025-97456-8","article-title":"SIRT1-based therapy targets a gene program involved in mitochondrial turnover in a model of retinal neurodegeneration","volume":"15","author":"Chaqour","year":"2025","journal-title":"Sci. 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