{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335424/"]},"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=GSE335424"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Bulk RNA sequencing reveals endothelial STING-dependent transcriptional programs in murine metabolic dysfunction-associated steatohepatitis","description":"Liver sinusoidal endothelial cells (LSECs) regulate nutrient flux and immune surveillance within the hepatic niche. Here, we investigate how endothelial-intrinsic cGAS-STING signaling integrates metabolic stress signals to reshape the hepatic niche in metabolic dysfunction-associated steatohepatitis (MASH). We performed bulk RNA sequencing on liver tissues from endothelial cell-specific Sting knockout mice (Stingfl/fl Cdh5-Cre+) and littermate controls (Stingfl/fl Cdh5-Cre-) subjected to a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 10 weeks. Gene set enrichment analysis revealed that multiple cancer-associated and fibrogenic signaling pathways were enriched in control livers but markedly suppressed in StingΔEC livers. Conversely, pathways related to T cell regulation and metabolism were preferentially enriched in StingΔEC livers, indicating that endothelial-intrinsic STING signaling drives MASH progression by reshaping T cell-mediated immune responses.","dates":{"publication":"2026/06/29"},"accession":"GSE335424","cross_references":{"GSM":["GSM9813476","GSM9813475","GSM9813477","GSM9813472","GSM9813474","GSM9813473"],"GPL":["24247"],"GSE":["335424"],"taxon":["Mus musculus"]}}