Recent Progress in Endothelial Senescence and Thrombosis: From Molecular Pathways to Therapeutic Prospects

Thrombosis constitutes the principal pathological basis for cardiovascular and cerebrovascular embolic events, with its incidence markedly escalating with advancing age. From a clinical perspective, thrombosis precipitates acute myocardial infarction, ischemic stroke, pulmonary embolism, and disseminated intravascular coagulation (DIC), conditions that frequently culminate in fatal outcomes. Increasing evidence suggests that senescent endothelial cells play a crucial role in mediating age-related thrombotic risk. Senescence-induced endothelial dysfunction compromises the cells' intrinsic anticoagulant capacity, while the acquisition of a senescence-associated secretory phenotype (SASP) further promotes a prothrombotic environment. Accordingly, endothelial cell senescence is integral to both the initiation and progression of thrombosis and its related pathologies. This review systematically summarizes the epidemiology of age-related thrombosis, elucidates the molecular underpinnings of endothelial cell senescence, and explores the intricate pathophysiological interplay between endothelial senescence and thrombosis. In addition, it provides a comprehensive overview of the molecular mechanisms, therapeutic strategies, and prospective targets relevant to vascular endothelial cell senescence, thereby offering new perspectives and theoretical foundations for the advancement of innovative anti-thrombotic interventions that specifically address aging-related pathophysiology.