{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE226nnn/GSE226668/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"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=GSE226668"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"RNA-Seq analysis TMAO effect on vascular smooth muscle cells","description":"Thoracic aneurysm/dissection (TAAD) is a life-threatening condition that lacks effective pharmacotherapeutic treatment. Vascular smooth muscle cells (VSMCs) phenotype switch and extracellular matrix (ECM) degradation has been thought to be critical to the development of TAAD. Trimethylamine N-oxide (TMAO), a metabolite produced by gut microorganisms, is tied with various risk factors for cardiovascular disease, however direct correlation with TAAD remains elusive. RNA-seq analysis TMAO targets identified a cohort of genes, critically involved in the ECM signaling.","dates":{"publication":"2026/06/30"},"accession":"GSE226668","cross_references":{"GSM":["GSM7081304","GSM7081305","GSM7081300","GSM7081301","GSM7081302","GSM7081303"],"GPL":["24247"],"GSE":["226668"],"taxon":["Mus musculus"]}}