Carotid Plaque‐Derived Small Extracellular Vesicles Mediate Atherosclerosis and Correlate With Plaque Vulnerability

the discovery cohort (n = 178) and an independent external cohort (n = 82). Mechanistic investigations identified miR-497-5p as a key mediator of vulnerable psEVs' proinflammatory and proatherogenic effects through directly targeting atheroprotective uncoupling protein 2 (UCP2). These findings highlight the roles of psEVs in atherogenesis and plaque vulnerability, providing valuable insights for risk stratification and therapeutic decision-making in aCAS patients.