Updated project metadata. Genotoxic stress in mammalian cells defined as a situation that initiates DNA damage compromising the cell’s genomic integrity leading to replication and transcription arrest underlies many pathological conditions including cellular senescence, cancer and cardiovascular diseases. Recent experimental data suggest that genotoxic stress in vitro induced by alkylating mutagen mitomycin C (MMC) is associated with proinflammatory activation of primary human endothelial cells and endothelial-to-mesenchymal transition, the key pathways underlying endothelial disfunction – an initial stage of atherosclerosis, a leading cause of cardiovascular morbidity and mortality worldwide. Given the increasing genotoxic load on the human organism from various environmental (ionizing and UV radiation) and anthropogenic (tobacco smoke, exhaust gases, industrial waste) sources, the decryption of molecular pathways underlying genotoxic stress induced endothelial dysfunction could improve our understanding of atherogenesis and help to justification of genotoxic stress as a novel risk factor for atherosclerosis. Therefore, we performed label-free proteomic profiling of Commercially available primary human coronary artery endothelial cells (HCAEC) and ) and internal thoracic artery endothelial cells (HITAEC) in vitro exposed to MMC followed by bioinformatic analysis to identify biochemical pathways and functional proteins underlying genotoxic stress induced endothelial dysfunction.