{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T15:10:58Z","timestamp":1777907458651,"version":"3.51.4"},"reference-count":36,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2023,12,29]],"date-time":"2023-12-29T00:00:00Z","timestamp":1703808000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hepatic ischemia\u2010reperfusion (IR) injury is a complex systemic process causing a series clinical problem. C\/EBP\u03b1 is a key transcription factor for hepatocyte function, but its role and mechanism in regulating hepatic IR injury are largely unknown. Occluding portal vein and hepatic artery was used to establish a mouse model of hepatic IR injury. C\/EBP\u03b1 expression was decreased in IR\u2010injured liver compared with the sham, accompanied by increased contents of serum alanine transaminase\u00a0(ALT), aspartate transaminase\u00a0(AST),\u00a0high mobility group box\u20101, and proportion of hepatic cells. Oxygen and glucose deprivation\/recovery (OGD\/R) was used to establish a cellular hepatic IR model in WRL\u201068 hepatocytes in vitro, and C\/EBP\u03b1 was overexpressed in the hepatocytes to evaluate its effect on hepatic IR injury. OGD\/R promoted oxidative stress, cell apoptosis and endoplasmic reticulum (ER) stress in hepatocytes, which was reversed by C\/EBP\u03b1 overexpression. Then, we found that C\/EBP\u03b1 promoted histone deacetylase 1 (HDAC1) transcription through binding to HDAC1 promoter. Moreover, HDAC1 deacetylated the activating transcription factor 4 (ATF4), a key positive regulator of ER\u00a0stress. Trichostatin\u2010A\u00a0(an HDAC inhibitor) or ATF4 overexpression reversed the improvement of C\/EBP\u03b1 on OGD\/R\u2010induced ER stress and hepatocyte dysfunction. 4\u2010Phenylbutyric acid\u00a0(an endoplasmic reticulum stress inhibitor) also reversed the hepatic IR injury induced by ATF4 overexpression. Finally, lentivirus\u2010mediated C\/EBP\u03b1 overexpression vector was applied to administrate hepatic IR mice, and the results showed that C\/EBP\u03b1 overexpression ameliorated IR\u2010induced\u00a0hepatic injury, manifesting with reduced ALT\/AST, oxidative stress and ER stress. Altogether, our findings suggested that C\/EBP\u03b1 ameliorated hepatic IR injury by inhibiting ER stress via HDAC1\u2010mediated deacetylation of ATF4 promoter.<\/jats:p>","DOI":"10.1002\/jbt.23630","type":"journal-article","created":{"date-parts":[[2023,12,29]],"date-time":"2023-12-29T03:59:47Z","timestamp":1703822387000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["C\/EBP\u03b1 alleviates hepatic ischemia\u2010reperfusion injury by inhibiting endoplasmic reticulum stress via HDAC1\u2010mediated deacetylation of ATF4"],"prefix":"10.1002","volume":"38","author":[{"given":"Rong","family":"Li","sequence":"first","affiliation":[{"name":"Department of Anesthesiology The Second Affiliated Hospital of Xi'an JiaoTong University  Xi'an People's Republic of China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Longbao","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of 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