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- W1034363480 abstract "Acetaminophen (APAP)-induced liver injury is a leading cause of drug-induced liver injury. Global hypoxia-inducible factor-1α (HIF-1α) deficiency transiently reduced APAP-induced liver injury in mice. The cellular source of HIF-1α that promotes APAP-induced liver injury is not known. We tested the hypothesis that activation of HIF-1α in hepatocytes promotes APAP-induced liver injury. Hepatocyte-specific HIF-1α-deficient mice (HIF-1αflox/flox/Albumin-Cre mice) and control mice (HIF-1αflox/flox mice) were treated with APAP (300 mg/kg, ip) and both liver injury and regeneration assessed 24 hours later. In contrast to global HIF-1α deficiency, hepatocyte HIF-1α deficiency did not reduce liver injury. Rather, liver injury was modestly increased in hepatocytes-pecific HIF-1α-deficient mice treatment. Moreover, hepatic cyclin D1 mRNA levels and the number of PCNA-positive hepatocytes was substantially reduced in hepatocyte specific-HIF-1α-deficient mice 24 hours after APAP administration, implicating HIF-1α as a promoter of liver regeneration after APAP overdose. Collectively, the results indicate that activation of HIF-1α in hepatocytes protects the liver after APAP exposure by promoting liver regeneration." @default.
- W1034363480 created "2016-06-24" @default.
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- W1034363480 date "2013-04-01" @default.
- W1034363480 modified "2023-09-23" @default.
- W1034363480 title "Hypoxia‐inducible factor‐1α activation in hepatocytes promotes liver regeneration after acetaminophen overdose" @default.
- W1034363480 doi "https://doi.org/10.1096/fasebj.27.1_supplement.257.4" @default.
- W1034363480 hasPublicationYear "2013" @default.
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