{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE310nnn/GSE310361/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE310361"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Gain- and loss-of-function RNA-seq analysis reveals DDIT4-driven transcriptional programs in human coronary artery smooth muscle cells","description":"This dataset profiles the transcriptomic changes resulting from DDIT4 manipulation in human coronary artery smooth muscle cells (HCASMCs). We performed RNA sequencing on HCASMCs following adenovirus-mediated DDIT4 overexpression or shRNA-mediated DDIT4 knockdown. Our analysis reveals that DDIT4 is both necessary and sufficient to drive a transcriptional program characteristic of VSMC dedifferentiation, establishing its critical role in phenotypic switching. These findings provide mechanistic insight into how this stress-responsive gene promotes proliferative arterial disease.","dates":{"publication":"2026/06/06"},"accession":"GSE310361","cross_references":{"GSM":["GSM9294629","GSM9294630","GSM9294631","GSM9294634","GSM9294635","GSM9294632","GSM9294633","GSM9294628"],"GPL":["23227"],"GSE":["310361"],"taxon":["Homo sapiens"]}}