<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE310nnn/GSE310361/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE310361</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Gain- and loss-of-function RNA-seq analysis reveals DDIT4-driven transcriptional programs in human coronary artery smooth muscle cells</name><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.</description><dates><publication>2026/06/06</publication></dates><accession>GSE310361</accession><cross_references><GSM>GSM9294629</GSM><GSM>GSM9294630</GSM><GSM>GSM9294631</GSM><GSM>GSM9294634</GSM><GSM>GSM9294635</GSM><GSM>GSM9294632</GSM><GSM>GSM9294633</GSM><GSM>GSM9294628</GSM><GPL>23227</GPL><GSE>310361</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>