<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315455/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315455</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Liver Endothelial Zonation Orchestrates Hepatic Steatosis Onset through Retinoic Acid-regulated FGF1</name><description>The contribution of liver sinusoidal endothelial cell (LSEC) zonation to metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis remains undefined. We identified selective lipid deposition in the pericentral zone during early MASLD. Multi-omics analyses confirmed enhanced pericentral lipid metabolism in both hepatocytes and LSECs. Mechanistically, pericentral LSEC marker c-Kit transcriptionally activated FGF1 via nuclear receptor RXRG, which suppressed hepatocellular lipid accumulation through FGFR4 signaling. Remarkably, retinoic acid (RXRG’s endogenous ligand and active vitamin A metabolite) phenocopied FGF1’s anti-steatotic effects. Clinical data revealed an inverse correlation between dietary vitamin A and MASLD severity, suggesting therapeutic potential of vitamin A supplementation for early intervention.</description><dates><publication>2026/05/05</publication></dates><accession>GSE315455</accession><cross_references><GSM>GSM9428992</GSM><GSM>GSM9428987</GSM><GSM>GSM9428988</GSM><GSM>GSM9428985</GSM><GSM>GSM9428986</GSM><GSM>GSM9428989</GSM><GSM>GSM9428990</GSM><GSM>GSM9428991</GSM><GPL>24247</GPL><GSE>315455</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>