{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T17:06:03Z","timestamp":1789923963794,"version":"4.0.1"},"reference-count":57,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2025,6,26]],"date-time":"2025-06-26T00:00:00Z","timestamp":1750896000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,6,26]],"date-time":"2025-06-26T00:00:00Z","timestamp":1750896000000},"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":["Aging Cell"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Lens epithelial cell (LEC) senescence is one of the key pathological processes of age\u2010related cataract (ARC) and is associated with oxidative stress, mitochondrial dysfunction, and protein aggregation. This study aimed to elucidate the pathogenesis of LEC senescence in ARC. The protein expression level of silencing regulatory protein 1 (SIRT1) and aptamer protein (p66Shc) was quantified. Reactive oxygen species (ROS) and mitochondrial superoxide levels were measured to evaluate cellular oxidative stress. Senescence\u2010associated protein expression (p21 and p53) and SA\u2010\u03b2\u2010galactosidase staining were employed to assess the aging status of LEC. Targeted metabolic analysis was conducted to explore energy changes during LEC senescence, and mitochondrial morphology and function were assessed in the cell models. The aging and damage conditions of the lens in ARC rats were evaluated through histological staining, transmission electron microscopy, expression of senescence\u2010related proteins, and oxidative stress markers. We comprehensively investigated the downregulation of SIRT1 expression and the upregulation of p66Shc expression in human cataract samples, UVB\u2010induced rat cataract models, and UVB\u2010treated LEC. SIRT1 could alleviate UVB\u2010induced oxidative stress, as well as mitochondrial dysfunction, inhibiting p66Shc expression in LEC. Nicotinamide mononucleotide (NMN) effectively alleviated the abnormal expression of aging\u2010related proteins and inhibited mitochondrial morphological and functional disorders by activating SIRT1. In conclusion, NMN activated SIRT1, inhibiting mitochondrial dysfunction, oxidative stress, and senescence in LEC, delaying lens opacity. This mechanism could be associated with the onset and progression of ARC, providing a new strategy for its prevention and treatment.<\/jats:p>","DOI":"10.1111\/acel.70155","type":"journal-article","created":{"date-parts":[[2025,6,26]],"date-time":"2025-06-26T11:20:18Z","timestamp":1750936818000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["<scp>SIRT1<\/scp>\n                    Prevents Lens Epithelial Cell Senescence During Age\u2010Related Cataract via Regulating\n                    <scp>p66Shc<\/scp>"],"prefix":"10.1111","volume":"24","author":[{"given":"Huirui","family":"Liu","sequence":"first","affiliation":[{"name":"Eye Hospital The First Affiliated Hospital of Harbin Medical University  Harbin China"},{"name":"NHC Key Laboratory of Cell Transplantation  Heilongjiang 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