{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T03:53:42Z","timestamp":1789098822093,"version":"build-2803163510"},"reference-count":60,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,2,9]],"date-time":"2025-02-09T00:00:00Z","timestamp":1739059200000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100012166","name":"National Key Research and Development Program of China","doi-asserted-by":"publisher","award":["2023YFC3603300"],"award-info":[{"award-number":["2023YFC3603300"]}],"id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82171558"],"award-info":[{"award-number":["82171558"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82471599"],"award-info":[{"award-number":["82471599"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["MedComm"],"published-print":{"date-parts":[[2025,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Alcohol\u2010associated liver disease (ALD) is a major cause of liver\u2010related morbidity and mortality, yet clinically effective therapies for ALD remain lacking. Here, we demonstrate that alcohol intake and its metabolite, acetaldehyde (ACH), induce senescence in the liver and liver cells, respectively. To assess the therapeutic potential of targeting liver senescence in ALD, we treated ALD\u2010affected mice with the senolytic compound ABT263 and the senomorphic NAD\n                    <jats:sup>+<\/jats:sup>\n                    precursor, nicotinamide (NAM). The results show that ABT263 effectively clears senescent hepatocytes and stellate cells, and reduces liver triglyceride (TG), but increases plasma alanine aminotransferase and TG levels. Conversely, NAM efficiently suppresses senescence and the senescence\u2010associated secretory phenotype (SASP), protecting the liver from alcohol\u2010induced injury in ALD mice. RNA\u2010sequencing analysis revealed that ABT263 treatment downregulated genes involved in adipogenesis while activating the complement pathway. In contrast, NAM upregulated metabolism\u2010related genes, such as\n                    <jats:italic>Sirt1<\/jats:italic>\n                    , and downregulated DNA damage marker genes, including\n                    <jats:italic>Rec8<\/jats:italic>\n                    and\n                    <jats:italic>E2f1<\/jats:italic>\n                    , in the liver. These findings suggest that cellular senescence plays a critical role in alcohol\u2010induced liver injury. Compared with senescent cell clearance by ABT263, suppressing senescence and SASP by NAM may provide a safer and more effective therapeutic approach for ALD.\n                  <\/jats:p>","DOI":"10.1002\/mco2.70086","type":"journal-article","created":{"date-parts":[[2025,2,11]],"date-time":"2025-02-11T01:41:04Z","timestamp":1739238064000},"source":"Crossref","is-referenced-by-count":16,"title":["Therapeutic potential of nicotinamide and ABT263 in alcohol\u2010associated liver disease through targeting cellular senescence"],"prefix":"10.1002","volume":"6","author":[{"given":"Naheemat Modupeola","family":"Gold","sequence":"first","affiliation":[{"name":"State Key Laboratory of Genetic Evolution &amp; Animal Models Key Laboratory of Healthy Aging Research of Yunnan Province Kunming Institute of Zoology Chinese Academy of Sciences  Kunming Yunnan China"},{"name":"Kunming College of Life Science University of Chinese Academy of Sciences  Kunming 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