{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T17:45:21Z","timestamp":1788371121190,"version":"build-2803163510"},"reference-count":40,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,1,27]],"date-time":"2025-01-27T00:00:00Z","timestamp":1737936000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,1,27]],"date-time":"2025-01-27T00:00:00Z","timestamp":1737936000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2025,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Age\u2010related cataracts (ARCs) are associated with increased oxidative stress and cellular senescence. Our objective is to investigate the function of Sirtuin 1 (SIRT1) within ARCs. In ARCs tissues and H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    \u2010treated lens epithelial cells (LECs), the expression levels of SIRT1 were examined. Senescence\u2010associated \u03b2\u2010galactosidase (SA\u2010\u03b2\u2010gal) staining was employed to evaluate cellular senescence. The Cell Counting Kit\u20108 assay was employed to measure viability. A wound healing assay was performed to assess migratory capacity in LECs. Oxidative stress\u2010related indicators were determined by enzyme\u2010linked immunosorbent assay kits. Additionally, the Coxpresdb and GeneCards databases were utilized to identify downstream pathways of SIRT1 in ARCs. The expression levels of protein and mRNA were detected using western blot and real\u2010time quantitative polymerase chain reaction, respectively. The expression of SIRT1 was downregulated in ARCs tissues with an increase in reactive oxygen species. In H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    \u2010induced LECs, SIRT1 was downregulated and its overexpression inhibited oxidative stress and cellular senescence while promoting viability and migration. Furthermore, FoxO1\/TLR4 pathway was screened out as the key pathway of SIRT1, which was activated in H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    \u2010induced LECs senescence. Overexpression of SIRT1 suppressed FoxO1\/TLR4 pathway. Further research demonstrated that the activation of FoxO1\/TLR4 pathway reversed the inhibitory role of SIRT1 in oxidative stress\u2010induced cellular senescence and the promotion effect of SIRT1 on viability and migration in H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    \u2010induced LECs. SIRT1 inhibits oxidative stress\u2010induced cellular senescence and promotes the viability and migration in H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    \u2010induced LECs via suppressing FoxO1\/TLR4 pathway.\n                  <\/jats:p>","DOI":"10.1002\/jbt.70150","type":"journal-article","created":{"date-parts":[[2025,1,27]],"date-time":"2025-01-27T03:54:09Z","timestamp":1737950049000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Sirtuin 1 Suppresses Hydrogen Peroxide\u2010Induced Senescence and Promotes Viability and Migration in Lens Epithelial Cells by Inhibiting Forkhead Box Protein O1\/Toll\u2010Like Receptor 4 Pathway"],"prefix":"10.1002","volume":"39","author":[{"given":"Hongda","family":"Jiang","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine The Affiliated Hospital of Southwest 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