{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T10:14:04Z","timestamp":1780395244227,"version":"3.54.1"},"reference-count":151,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2023,12,23]],"date-time":"2023-12-23T00:00:00Z","timestamp":1703289600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Institutes of Health (NIH)","award":["R01 ES016541"],"award-info":[{"award-number":["R01 ES016541"]}]},{"name":"National Institutes of Health (NIH)","award":["R01 ES 030374"],"award-info":[{"award-number":["R01 ES 030374"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Toxics"],"abstract":"<jats:p>Prenatal exposure to endocrine disruptors such as bisphenol A (BPA) plays a critical role in the developmental programming of liver dysfunction that is characteristic of nonalcoholic fatty liver disease (NAFLD). Circadian and aging processes have been implicated in the pathogenesis of NAFLD. We hypothesized that the prenatal BPA-induced fatty-liver phenotype of female sheep is associated with premature hepatic senescence and disruption in circadian clock genes. The expression of circadian rhythm and aging-associated genes, along with other markers of senescence such as telomere length, mitochondrial DNA copy number, and lipofuscin accumulation, were evaluated in the liver tissue of control and prenatal BPA groups. Prenatal BPA exposure significantly elevated the expression of aging-associated genes GLB1 and CISD2 and induced large magnitude differences in the expression of other aging genes\u2014APOE, HGF, KLOTHO, and the clock genes PER2 and CLOCK\u2014in the liver; the other senescence markers remained unaffected. Prenatal BPA-programmed aging-related transcriptional changes in the liver may contribute to pathological changes in liver function, elucidating the involvement of aging genes in the pathogenesis of liver steatosis.<\/jats:p>","DOI":"10.3390\/toxics12010015","type":"journal-article","created":{"date-parts":[[2023,12,24]],"date-time":"2023-12-24T20:42:30Z","timestamp":1703450550000},"page":"15","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Developmental Programming: Impact of Prenatal Exposure to Bisphenol A on Senescence and Circadian Mediators in the Liver of Sheep"],"prefix":"10.3390","volume":"12","author":[{"given":"Giuliana","family":"Motta","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Michigan, Ann Arbor, MI 48105, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soundara Viveka","family":"Thangaraj","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Michigan, Ann Arbor, MI 48105, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8443-7212","authenticated-orcid":false,"given":"Vasantha","family":"Padmanabhan","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Michigan, Ann Arbor, MI 48105, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,12,23]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"841","DOI":"10.3350\/cmh.2022.0239","article-title":"Forecasted 2040 global prevalence of nonalcoholic fatty liver disease using hierarchical bayesian approach","volume":"28","author":"Le","year":"2022","journal-title":"Clin. 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