<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/GSE311nnn/GSE311133/</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=GSE311133</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptome analysis of human coronary artery smooth muscle cells under pro-differentiation and pro-dedifferentiation treatments</name><description>This study explores the transcriptomic landscape of human coronary artery smooth muscle cells (HCASMCs) in response to stimuli that promote differentiation (Repsox) or dedifferentiation (PDGF-BB, IL-1b). Our RNA sequencing analysis identifies DNA damage-inducible transcript 4 (DDIT4) as a key regulator of vascular smooth muscle cell (VSMC) phenotypic switching, showing its significant upregulation in synthetic phenotypes and downregulation in contractile phenotypes. This dataset provides a resource for understanding the transcriptional programs governing VSMC plasticity in the context of vascular remodeling and atherosclerotic disease.</description><dates><publication>2026/06/06</publication></dates><accession>GSE311133</accession><cross_references><GSM>GSM9317519</GSM><GSM>GSM9317529</GSM><GSM>GSM9317518</GSM><GSM>GSM9317517</GSM><GSM>GSM9317528</GSM><GSM>GSM9317516</GSM><GSM>GSM9317527</GSM><GSM>GSM9317515</GSM><GSM>GSM9317526</GSM><GSM>GSM9317525</GSM><GSM>GSM9317524</GSM><GSM>GSM9317523</GSM><GSM>GSM9317522</GSM><GSM>GSM9317521</GSM><GSM>GSM9317520</GSM><GPL>23227</GPL><GSE>311133</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>