{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339100/"]},"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=GSE339100"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"sc-RNAseq of glomerular cells in a mouse model of malignant hypertension","description":"Hypertensive emergency (HTEM) is defined by abrupt blood pressure elevation with acute multi‑organ damage, yet the mechanisms predisposing only a subset of hypertensive individuals to HTEM remain unclear. Progress has been limited by the lack of a mouse model that faithfully replicates human disease. We aimed to identify determinants of susceptibility to hypertensive microvascular injury and characterize a murine model of HTEM. Males 129S2/SvPasCrl (129Sv) mice were exposed to severe hypertension via angiotensin II infusion combined with a high‑salt diet wth or withour supplementation with rhPlGF2. We assessed glomerular transcriptional profiles using single‑cell RNA sequencing. Single‑cell transcriptomics revealed profound repression of angiogenic, metabolic, and stress-response pathways in glomerular endothelial cells, a repression partially restored by rhPlGF-2.","dates":{"publication":"2026/09/01"},"accession":"GSE339100","cross_references":{"GSM":["GSM9888482","GSM9888483","GSM9888480","GSM9888481","GSM9888479","GSM9888477","GSM9888478"],"GPL":["30172"],"GSE":["339100"],"taxon":["Mus musculus"]}}