GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335775/primary200OKTranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE335775GEOGSEfalseSingle-cell RNA sequencing reveals endothelial STING-dependent immune remodeling in murine metabolic dysfunction-associated steatohepatitisLiver 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 adaptive immune responses in metabolic dysfunction-associated steatohepatitis (MASH) at single-cell resolution. We performed single-cell 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 western diet combined with CCl4 (WD-CCl4) for 12 weeks. Unbiased cell-type annotation revealed broad immune remodeling following LSEC-STING deletion. Among CD4+ T cells, LSEC-STING deletion resulted in a marked reduction of pathological Th17 cells, accompanied by expansion of regulatory T cells (Tregs), leading to a significantly increased Treg/Th17 ratio. LSEC-STING deletion also reduced exhausted CD8+ T cells while increasing effector CD8+ T cells. Mechanistically, LSEC-intrinsic STING signaling represses BMP4 transcription through NF-kB-mediated competition with AP-1, disrupting a tolerance-supporting angiocrine program. These findings identify endothelial STING as a vascular immunometabolic checkpoint that links chronic metabolic stress to adaptive immune remodeling in MASH.2026/06/29GSE335775GSM9820635GSM9820636GSM9820634GSM9820639GSM9820637GSM982063828330335775Mus musculus