{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T12:46:51Z","timestamp":1791550011662,"version":"4.3.4"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","license":[{"start":{"date-parts":[[2022,6,30]],"date-time":"2022-06-30T00:00:00Z","timestamp":1656547200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background and Aims<\/jats:title>\n            <jats:p>Hydrogen sulfide (H<jats:sub>2<\/jats:sub>S) plays a protective role in NAFLD. However, whether cystathionine \u03b3 lyase (CSE), a dominant H<jats:sub>2<\/jats:sub>S generating enzyme in hepatocytes, has a role in the pathogenesis of NAFLD is currently unclear.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results<\/jats:title>\n            <jats:p>We showed that CSE protein expression is dramatically downregulated, especially in fibrotic areas, in livers from patients with NAFLD. In high\u2010fat diet (HFD)\u2010induced NAFLD mice or an oleic acid\u2010induced hepatocyte model, the CSE\/H<jats:sub>2<\/jats:sub>S pathway is also downregulated. To illustrate a regulatory role for CSE in NAFLD, we generated a hepatocyte\u2010specific <jats:italic toggle=\"yes\">CSE<\/jats:italic> knockout mouse (<jats:italic toggle=\"yes\">CSE<\/jats:italic>\n                                 <jats:sup>LKO<\/jats:sup>). Feeding an HFD to <jats:italic toggle=\"yes\">CSE<\/jats:italic>\n                                 <jats:sup>LKO<\/jats:sup> mice, they showed more hepatic lipid deposition with increased activity of the fatty acid de novo synthesis pathway, increased hepatic insulin resistance, and higher hepatic gluconeogenic ability compared to <jats:italic toggle=\"yes\">CSE<\/jats:italic>\n                                 <jats:sup>Loxp<\/jats:sup> control mice. By contrast, H<jats:sub>2<\/jats:sub>S donor treatment attenuated these phenotypes. Furthermore, the protection conferred by H<jats:sub>2<\/jats:sub>S was blocked by farnesoid X receptor (<jats:italic toggle=\"yes\">FXR<\/jats:italic>) knockdown. Consistently, serum deoxycholic acid and lithocholic acid (FXR antagonists) were increased, and tauro\u2010\u03b2\u2010muricholic acid (FXR activation elevated) was reduced in CSE<jats:sup>LKO<\/jats:sup>. CSE\/H<jats:sub>2<\/jats:sub>S promoted a post\u2010translation modification (sulfhydration) of FXR at Cys138\/141 sites, thereby enhancing its activity to modulate expression of target genes related to lipid and glucose metabolism, inflammation, and fibrosis. Sulfhydration proteomics in patients' livers supported the CSE\/H<jats:sub>2<\/jats:sub>S modulation noted in the <jats:italic toggle=\"yes\">CSE<\/jats:italic>\n                                 <jats:sup>LKO<\/jats:sup> mice.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>FXR sulfhydration is a post\u2010translational modification affected by hepatic endogenous CSE\/H<jats:sub>2<\/jats:sub>S that may promote FXR activity and attenuate NAFLD. Hepatic CSE deficiency promotes development of nonalcoholic steatohepatitis. The interaction between H<jats:sub>2<\/jats:sub>S and FXR may be amenable to therapeutic drug treatment in NAFLD.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.32577","type":"journal-article","created":{"date-parts":[[2022,5,19]],"date-time":"2022-05-19T08:05:40Z","timestamp":1652947540000},"page":"1794-1810","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":83,"title":["Hepatocellular cystathionine \u03b3 lyase\/hydrogen sulfide attenuates nonalcoholic fatty liver disease by activating farnesoid X receptor"],"prefix":"10.1097","volume":"76","author":[{"given":"Wenjing","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Pathology, School of Basic Medical Science,Xi'an Medical University,Shanxi,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changting","family":"Cui","sequence":"additional","affiliation":[{"name":"Hypertension Center, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases,Fuwai Hospital of Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunmei","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Bioinformatics, Physiology and Pathophysiology, School of Basic Medical Sciences,Peking University,Beijing,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenzhen","family":"Chen","sequence":"additional","affiliation":[{"name":"Hypertension Center, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases,Fuwai Hospital of Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haizeng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Hypertension Center, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases,Fuwai Hospital of Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qinghua","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Bioinformatics, Physiology and Pathophysiology, School of Basic Medical Sciences,Peking University,Beijing,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guoheng","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Bioinformatics, Physiology and Pathophysiology, School of Basic Medical Sciences,Peking University,Beijing,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianglin","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Pathology, School of Basic Medical Science,Xi'an Medical University,Shanxi,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Gastrointestinal Surgery,the First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liangjie","family":"Tang","sequence":"additional","affiliation":[{"name":"NAFLD Research Center, Department of Hepatology,the First Affiliated Hospital of Wenzhou Medical University; the Key Laboratory of Diagnosis and Treatment for the Development of Chronic Liver Disease in Zhejiang Province,Wenzhou,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4325-3900","authenticated-orcid":false,"given":"Giovanni","family":"Targher","sequence":"additional","affiliation":[{"name":"Section of Endocrinology, Diabetes and Metabolism, Department of Medicine,University and Azienda Ospedaliera Universitaria Integrata of Verona,Verona,Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6322-7753","authenticated-orcid":false,"given":"Christopher D.","family":"Byrne","sequence":"additional","affiliation":[{"name":"Southampton National Institute for Health and Care Research Biomedical Research Centre,University Hospital Southampton, Southampton General Hospital,Southampton,UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4984-2631","authenticated-orcid":false,"given":"Ming\u2010Hua","family":"Zheng","sequence":"additional","affiliation":[{"name":"NAFLD Research Center, Department of Hepatology,the First Affiliated Hospital of Wenzhou Medical University; the Key Laboratory of Diagnosis and Treatment for the Development of Chronic Liver Disease in Zhejiang Province,Wenzhou,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liming","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology,Harbin Medical University\u2010Daqing,Daqing,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Cai","sequence":"additional","affiliation":[{"name":"Hypertension Center, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases,Fuwai Hospital of Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7573-8710","authenticated-orcid":false,"given":"Bin","family":"Geng","sequence":"additional","affiliation":[{"name":"Hypertension Center, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases,Fuwai Hospital of Chinese Academy of Medical Sciences and Peking Union Medical 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