{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T02:38:07Z","timestamp":1784774287514,"version":"3.55.0"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2021,9,25]],"date-time":"2021-09-25T00:00:00Z","timestamp":1632528000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims<\/jats:title>\n            <jats:p>Hepatocellular dedifferentiation is emerging as an important determinant in liver disease progression. Preservation of mature hepatocyte identity relies on a set of key genes, predominantly the transcription factor hepatocyte nuclear factor 4\u03b1 (HNF4\u03b1) but also splicing factors like SLU7. How these factors interact and become dysregulated and the impact of their impairment in driving liver disease are not fully understood.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results<\/jats:title>\n            <jats:p>Expression of <jats:italic toggle=\"yes\">SLU7<\/jats:italic> and that of the adult and oncofetal isoforms of <jats:italic toggle=\"yes\">HNF4\u03b1<\/jats:italic>, driven by its promoter 1 (P1) and P2, respectively, was studied in diseased human and mouse livers. Hepatic function and damage response were analyzed in wild\u2010type and <jats:italic toggle=\"yes\">Slu7<\/jats:italic>\u2010haploinsufficient\/heterozygous (<jats:italic toggle=\"yes\">Slu7+\/\u2212\n                                 <\/jats:italic>) mice undergoing chronic (CCl<jats:sub>4<\/jats:sub>) and acute (acetaminophen) injury. SLU7 expression was restored in CCl<jats:sub>4<\/jats:sub>\u2010injured mice using SLU7\u2010expressing adeno\u2010associated viruses (AAV\u2010SLU7). The hepatocellular SLU7 interactome was characterized by mass spectrometry. Reduced <jats:italic toggle=\"yes\">SLU7<\/jats:italic> expression in human and mouse diseased livers correlated with a switch in <jats:italic toggle=\"yes\">HNF4\u03b1<\/jats:italic> P1 to P2 usage. This response was reproduced in <jats:italic toggle=\"yes\">Slu7+\/\u2212\n                                 <\/jats:italic> mice, which displayed increased sensitivity to chronic and acute liver injury, enhanced oxidative stress, and marked impairment of hepatic functions. AAV\u2010SLU7 infection prevented liver injury and hepatocellular dedifferentiation. Mechanistically we demonstrate a unique role for SLU7 in the preservation of HNF4\u03b11 protein stability through its capacity to protect the liver against oxidative stress. SLU7 is herein identified as a key component of the stress granule proteome, an essential part of the cell\u2019s antioxidant machinery.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Our results place SLU7 at the highest level of hepatocellular identity control, identifying SLU7 as a link between stress\u2010protective mechanisms and liver differentiation. These findings emphasize the importance of the preservation of hepatic functions in the protection from liver injury.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.32029","type":"journal-article","created":{"date-parts":[[2021,6,25]],"date-time":"2021-06-25T11:32:23Z","timestamp":1624620743000},"page":"2791-2807","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":24,"title":["Splicing Factor SLU7 Prevents Oxidative Stress\u2010Mediated Hepatocyte Nuclear Factor 4\u03b1 Degradation, Preserving Hepatic Differentiation and Protecting From Liver Damage"],"prefix":"10.1097","volume":"74","author":[{"given":"Mar\u00eda","family":"G\u00e1rate\u2010Rasc\u00f3n","sequence":"first","affiliation":[{"name":"Hepatology Program,CIMA,University of Navarra,Pamplona,Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miriam","family":"Recalde","sequence":"additional","affiliation":[{"name":"Hepatology Program,CIMA,University of Navarra,Pamplona,Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maddalen","family":"Jimenez","sequence":"additional","affiliation":[{"name":"Hepatology Program,CIMA,University of Navarra,Pamplona,Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mar\u00eda","family":"Elizalde","sequence":"additional","affiliation":[{"name":"Hepatology Program,CIMA,University of Navarra,Pamplona,Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mar\u00eda","family":"Azkona","sequence":"additional","affiliation":[{"name":"Hepatology Program,CIMA,University of Navarra,Pamplona,Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iker","family":"Uriarte","sequence":"additional","affiliation":[{"name":"Hepatology Program,CIMA,University of Navarra,Pamplona,Spain"},{"name":"CIBERehd,Instituto de Salud Carlos III,Madrid,Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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