{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE311nnn/GSE311116/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311116"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"DDIT4 overexpression reshapes the histone modification landscape in human coronary artery smooth muscle cells: an H3K9ac and H3K27ac CUT&Tag study","description":"This study investigates the epigenetic mechanisms by which DDIT4 promotes vascular smooth muscle cell (VSMC) dedifferentiation. We performed CUT&Tag sequencing for the active histone marks H3K9ac and H3K27ac in HCASMCs following DDIT4 overexpression. Our findings reveal that DDIT4, by inhibiting the pyruvate dehydrogenase complex, reduces acetyl-CoA levels and globally decreases histone acetylation. Specifically, we observe loss of H3K9ac and H3K27ac at the promoters of key contractile genes, providing an epigenetic explanation for the DDIT4-mediated suppression of the contractile phenotype and acceleration of atherosclerosis.","dates":{"publication":"2026/06/06"},"accession":"GSE311116","cross_references":{"GSM":["GSM9317297","GSM9317296","GSM9317295","GSM9317294","GSM9317293","GSM9317292","GSM9317291","GSM9317290","GSM9317289","GSM9317300","GSM9317299","GSM9317298"],"GPL":["34284"],"GSE":["311116"],"taxon":["Homo sapiens"]}}