GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE323nnn/GSE323983/primary200OKTranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE323983GEOGSEfalseSenescence inhibition by rapamycin mitigates radiation-induced atherosclerotic characteristics in human coronary endothelial cellsIonising radiation (IR) is a recognised risk factor for cardiovascular disease (CVD), yet the mechanisms linking it to exposure remain incompletely understood. We show that IR drives a pro-atherogenic phenotype in human coronary artery endothelial cells (HCAECs) through the induction of cellular senescence, and that rapamycin attenuates these effects. IR triggered hallmark senescence features, including elevated SA-β-galactosidase activity, nuclear enlargement, and increased CDKN1A and p53 expression. Functionally, irradiated HCAECs displayed impaired barrier integrity and heightened monocyte adhesion. Transcriptomic and proteomic profiling revealed broad IR-induced alterations enriched in DNA damage response, cell-cycle arrest, senescence, proteostasis, and immune-related pathways. These findings establish a mechanistic link between radiation-induced endothelial senescence and early atherogenic-associated dysfunction, demonstrating that senescence is a driver of vascular injury. Importantly, identifying mTOR inhibition as a promising strategy to counteract radiation-associated endothelial dysfunction. This work positions senescence as a tractable therapeutic target in radiation-induced vascular injury.2026/06/24GSE323983GSM9566095GSM9566084GSM9566072GSM9566093GSM9566082GSM9566091GSM9566080GSM9566108GSM9566107GSM9566105GSM9566114GSM9566103GSM9566112GSM9566101GSM9566078GSM9566089GSM9566110GSM9566099GSM9566087GSM9566076GSM9566097GSM9566086GSM956607428975323983Homo sapiens