{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang X"],"funding":["Food and Health Bureau of the Government of the Hong Kong Special Administrative Region | Health and Medical Research Fund (HMRF)","Research Grants Council, University Grants Committee (RGC, UGC)","National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund)"],"pagination":["102-119"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11774752"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(1)"],"pubmed_abstract":["Transmembrane-6 superfamily member 2 (TM6SF2) regulates hepatic fat metabolism and is associated with metabolic dysfunction-associated steatohepatitis (MASH). TM6SF2 genetic variants are associated with steatotic liver disease. The pathogenesis of MASH involves genetic factors and gut microbiota alteration, yet the role of host-microbe interactions in MASH development remains unclear. Here, we discover that mice with intestinal epithelial cell-specific knockout of Tm6sf2 (Tm6sf2<sup>ΔIEC</sup>) develop MASH, accompanied by impaired intestinal barrier and microbial dysbiosis. Transplanting stools from Tm6sf2<sup>ΔIEC</sup> mice induces steatohepatitis in germ-free recipient mice, whereas MASH is alleviated in Tm6sf2<sup>ΔIEC</sup> mice co-housed with wild-type mice. Mechanistically, Tm6sf2-"],"journal":["Nature metabolism"],"pubmed_title":["Intestinal TM6SF2 protects against metabolic dysfunction-associated steatohepatitis through the gut-liver axis."],"pmcid":["PMC11774752"],"funding_grant_id":["14117422 and 14117123","08191336","T12-703/19-R","82222901, 82103355 and 82272619"],"pubmed_authors":["Wu J","Pan Y","Ji F","Lau HC","Wong CC","Zhou Y","Xu H","Yu J","Ha S","Lee HW","Zhao Y","Liang C","Li X","Wong VW","Zhang Y","Zhang X","Ng QW","Cheung AHK","Liu C","Song Y","Lo JCY"],"additional_accession":[]},"is_claimable":false,"name":"Intestinal TM6SF2 protects against metabolic dysfunction-associated steatohepatitis through the gut-liver axis.","description":"Transmembrane-6 superfamily member 2 (TM6SF2) regulates hepatic fat metabolism and is associated with metabolic dysfunction-associated steatohepatitis (MASH). TM6SF2 genetic variants are associated with steatotic liver disease. The pathogenesis of MASH involves genetic factors and gut microbiota alteration, yet the role of host-microbe interactions in MASH development remains unclear. Here, we discover that mice with intestinal epithelial cell-specific knockout of Tm6sf2 (Tm6sf2<sup>ΔIEC</sup>) develop MASH, accompanied by impaired intestinal barrier and microbial dysbiosis. Transplanting stools from Tm6sf2<sup>ΔIEC</sup> mice induces steatohepatitis in germ-free recipient mice, whereas MASH is alleviated in Tm6sf2<sup>ΔIEC</sup> mice co-housed with wild-type mice. Mechanistically, Tm6sf2-","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-02T01:52:20.89Z","creation":"2025-04-07T04:18:27.058Z"},"accession":"S-EPMC11774752","cross_references":{"pubmed":["39779889"],"doi":["10.1038/s42255-024-01177-7"]}}