{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315455/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315455"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Liver Endothelial Zonation Orchestrates Hepatic Steatosis Onset through Retinoic Acid-regulated FGF1","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.","dates":{"publication":"2026/05/05"},"accession":"GSE315455","cross_references":{"GSM":["GSM9428992","GSM9428987","GSM9428988","GSM9428985","GSM9428986","GSM9428989","GSM9428990","GSM9428991"],"GPL":["24247"],"GSE":["315455"],"taxon":["Mus musculus"]}}