Telomere shortening and endothelial cell senescence are linked to atherosclerosis. This study shows that senescent endothelial cells are present in human atherosclerotic lesions and may contribute to atherogenesis. Senescent vascular cells were identified by β-galactosidase activity in coronary arteries but not in internal mammary arteries. Immunohistochemistry confirmed that β-gal-positive cells were endothelial cells. Senescent endothelial cells exhibited increased expression of intercellular adhesion molecule-1 (ICAM-1) and decreased endothelial nitric oxide synthase (eNOS) activity, both of which are implicated in atherogenesis. Telomerase activation prevented these functional changes in endothelial cells. The study suggests that telomere shortening contributes to endothelial dysfunction and atherogenesis. Telomerase may be a potential therapeutic target for preventing atherosclerosis. The findings highlight the role of telomere function in vascular health and aging.Telomere shortening and endothelial cell senescence are linked to atherosclerosis. This study shows that senescent endothelial cells are present in human atherosclerotic lesions and may contribute to atherogenesis. Senescent vascular cells were identified by β-galactosidase activity in coronary arteries but not in internal mammary arteries. Immunohistochemistry confirmed that β-gal-positive cells were endothelial cells. Senescent endothelial cells exhibited increased expression of intercellular adhesion molecule-1 (ICAM-1) and decreased endothelial nitric oxide synthase (eNOS) activity, both of which are implicated in atherogenesis. Telomerase activation prevented these functional changes in endothelial cells. The study suggests that telomere shortening contributes to endothelial dysfunction and atherogenesis. Telomerase may be a potential therapeutic target for preventing atherosclerosis. The findings highlight the role of telomere function in vascular health and aging.