{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T11:59:11Z","timestamp":1781870351240,"version":"3.54.5"},"reference-count":70,"publisher":"SAGE Publications","issue":"10-12","license":[{"start":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T00:00:00Z","timestamp":1769472000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Beijing Natural Science Foundation","award":["7264252"],"award-info":[{"award-number":["7264252"]}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2026,4,1]]},"abstract":"<jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>Cataracts are the leading cause of blindness worldwide, and the mechanism underlying cataract formation is linked to the oxidative damage and the apoptosis of lens epithelial cells. Retinoic acid Receptor\u2010related orphan receptor \u03b1 (ROR\u03b1), a transcription factor, prevents oxidative stress and cell apoptosis. ROR\u03b1 is decreased in the lens from patients with cataract, but it remains unclear whether decreases in ROR\u03b1 are attributed to cataract formation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Here, rat models of selenite-induced cataracts were used for\n                      <jats:italic toggle=\"yes\">in\u00a0vivo<\/jats:italic>\n                      experiments.\n                      <jats:italic toggle=\"yes\">In vitro<\/jats:italic>\n                      , human lens epithelial cells (SRA01-04) were treated with selenite. ROR\u03b1 was downregulated in the lens from rat models of selenite-induced cataracts. The ROR\u03b1 agonist SR1078 significantly mitigated the degree of lens opacity. SR1078 reduced oxidative stress, cell apoptosis, and mitochondrial dysfunction and promoted the peroxisome proliferative activated receptor gamma coactivator (PGC-1\u03b1) and the nuclear factor erythroid 2-related factor 2 (Nrf2)-heme oxygenase-1 pathways in the lens from rat models of selenite-induced cataracts and lens epithelial cells upon selenite stimulation. ROR\u03b1 overexpression showed a similar protective effect on lens epithelial cells\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      . Nerve growth factor (NGF) expression was up-regulated by ROR\u03b1 overexpression. Although ROR\u03b1 overexpression prevented selenite-induced damage to lens epithelial cells, the damage recurred following NGF knockdown.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>\n                      ROR\u03b1 protects against selenite-induced oxidative stress and cellular apoptosis. In the context of cataractogenesis, NGF is newly identified as a transcriptional target of ROR\u03b1, and its reduction is related to mitochondrial dysfunction in lens epithelial cells. Our study highlights the translational potential of ROR\u03b1 activation as a nonsurgical cataract intervention.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      44, 599\u2013617.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/15230864261416452","type":"journal-article","created":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T03:53:46Z","timestamp":1769572426000},"page":"599-617","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["Targeting Retinoic Acid Receptor-Related Orphan Receptor \u03b1 to Prevent Cataracts: A New Pathway Through Nerve Growth Factor Activation"],"prefix":"10.1177","volume":"44","author":[{"given":"Zhenyu","family":"Wang","sequence":"first","affiliation":[{"name":"Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Capital Medical University, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinda","family":"Wang","sequence":"additional","affiliation":[{"name":"Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Capital Medical University, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuemin","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Peking University Third Hospital, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Wan","sequence":"additional","affiliation":[{"name":"Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Capital Medical University, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Tao","sequence":"additional","affiliation":[{"name":"Beijing Tongren Eye Center, Beijing Tongren Hospital, Beijing Key Laboratory of Ophthalmology and Visual Sciences, Capital Medical University, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,1,27]]},"reference":[{"key":"e_1_3_3_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2004.05.011"},{"key":"e_1_3_3_3_1","doi-asserted-by":"publisher","DOI":"10.1210\/mend.13.9.0343"},{"key":"e_1_3_3_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/cbf.1737"},{"key":"e_1_3_3_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbc.2021.101358"},{"key":"e_1_3_3_6_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00531.2018"},{"key":"e_1_3_3_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/febs.13729"},{"key":"e_1_3_3_8_1","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.12-10816"},{"key":"e_1_3_3_9_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.877544"},{"key":"e_1_3_3_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.exer.2008.05.018"},{"key":"e_1_3_3_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/s0014-4835(81)80125-x"},{"key":"e_1_3_3_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/hep.27577"},{"key":"e_1_3_3_13_1","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2022.829067"},{"key":"e_1_3_3_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2012.05.019"},{"key":"e_1_3_3_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.aopr.2021.100008"},{"key":"e_1_3_3_16_1","doi-asserted-by":"publisher","DOI":"10.1021\/acsinfecdis.0c00107"},{"issue":"3","key":"e_1_3_3_17_1","first-page":"273","article-title":"Superoxide dismutase activity in cataractous lenses","volume":"36","author":"Fujiwara H","year":"1992","unstructured":"Fujiwara H, , Takigawa Y, , Suzuki T, et al. 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