{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T22:28:59Z","timestamp":1789684139176,"version":"4.0.1"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2018,3,23]],"date-time":"2018-03-23T00:00:00Z","timestamp":1521763200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hepatology Communications"],"published-print":{"date-parts":[[2018,5]]},"abstract":"<jats:p>The mechanisms by which the liver fails in end\u2010stage liver disease remain elusive. Disruption of the transcription factor network in hepatocytes has been suggested to mediate terminal liver failure in animals. However, this hypothesis remains unexplored in human subjects. To study the relevance of transcription factor expression in terminal stages of chronic liver failure in humans, we analyzed the expression of liver\u2010enriched transcription factors (LETFs) hepatocyte nuclear factor (HNF)4\u03b1, HNF1\u03b1, forkhead box protein A2 (FOXA2), CCAAT\/enhancer\u2010binding protein (CEBP)\u03b1, and CEBP\u03b2. We then selected downstream genes responsible for some hepatic functions (ornithine transcarbamylase [OTC], cytochrome P450 3A4 [CYP3A4], coagulation factor VII [F7], cadherin 1 [CDH1], phospho\u2010ezrin (Thr567)\/radixin (Thr564)\/moesin (Thr558) [p\u2010ERM], phospho\u2010myosin light chain [p\u2010MLC], low\u2010density lipoprotein receptor\u2010related protein 1 [LRP1]) in liver tissue from patients at different stages of decompensated liver function based upon Child\u2010Pugh classification, Model for End\u2010Stage Liver Disease score, and degree of inflammatory activity\/fibrosis. We first examined differential expression of LETF and determined whether a relationship exists between transcript and protein expression, and liver function. We found HNF4\u03b1 expression was down\u2010regulated and correlated well with the extent of liver dysfunction (<jats:italic toggle=\"yes\">P =<\/jats:italic>0.001), stage of fibrosis (<jats:italic toggle=\"yes\">P =<\/jats:italic>0.0005), and serum levels of total bilirubin (<jats:italic toggle=\"yes\">P =<\/jats:italic>0.009;<jats:italic toggle=\"yes\">r =<\/jats:italic>0.35), albumin (<jats:italic toggle=\"yes\">P<\/jats:italic>&lt; 0.001;<jats:italic toggle=\"yes\">r =<\/jats:italic>0.52), and prothrombin time activity (<jats:italic toggle=\"yes\">P =<\/jats:italic>0.002;<jats:italic toggle=\"yes\">r =<\/jats:italic>0.41). HNF4\u03b1 expression also correlated with CYP3A4, OTC, and F7 as well as CDH1 RNA levels. The Rho\/Rho\u2010associated protein kinase pathways, which have been implicated in the regulation of HNF4\u03b1, were also differentially expressed, in concert with LRP1, a reported upstream regulator of RhoA function.<jats:italic toggle=\"yes\">Conclusion:<\/jats:italic>HNF4\u03b1 and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. (<jats:italic toggle=\"yes\">Hepatology Communications<\/jats:italic>2018;2:582\u2010594)<\/jats:p>","DOI":"10.1002\/hep4.1172","type":"journal-article","created":{"date-parts":[[2018,3,23]],"date-time":"2018-03-23T19:03:21Z","timestamp":1521831801000},"page":"582-594","source":"Crossref","is-referenced-by-count":37,"title":["Liver\u2010enriched transcription factor expression relates to chronic hepatic failure in humans"],"prefix":"10.1097","volume":"2","author":[{"given":"Jorge","family":"Guzman\u2010Lepe","sequence":"first","affiliation":[{"name":"Department of Pathology,University of Pittsburgh,Pittsburgh,PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eduardo","family":"Cervantes\u2010Alvarez","sequence":"additional","affiliation":[{"name":"Department of Pathology,University of Pittsburgh,Pittsburgh,PA"},{"name":"PECEM, Facultad de Medicina,Universidad Nacional Aut\u00f3noma de M\u00e9xico,Mexico 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University,Fukuoka,Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuki","family":"Bekki","sequence":"additional","affiliation":[{"name":"Department of Surgery and Science, Graduate School of Medical Sciences,Kyushu University,Fukuoka,Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masahiro","family":"Shimokawa","sequence":"additional","affiliation":[{"name":"Department of Surgery and Science, Graduate School of Medical Sciences,Kyushu University,Fukuoka,Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huanlin","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Surgery and Science, Graduate School of Medical Sciences,Kyushu University,Fukuoka,Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomoharu","family":"Yoshizumi","sequence":"additional","affiliation":[{"name":"Department of Surgery and Science, Graduate School of Medical Sciences,Kyushu University,Fukuoka,Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshihiko","family":"Maehara","sequence":"additional","affiliation":[{"name":"Department of Surgery and Science, Graduate School of Medical Sciences,Kyushu University,Fukuoka,Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aaron","family":"Bell","sequence":"additional","affiliation":[{"name":"Department of Pathology,University of Pittsburgh,Pittsburgh,PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ira J.","family":"Fox","sequence":"additional","affiliation":[{"name":"Department of Surgery,Children's Hospital of Pittsburgh of the University of Pittsburgh Medical Center,Pittsburgh,PA"},{"name":"McGowan Institute for Regenerative Medicine,University of Pittsburgh,Pittsburgh,PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuki","family":"Takeishi","sequence":"additional","affiliation":[{"name":"Department of Pathology,University of 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