Cardiovascular diseases pose a serious threat to public health, and their prevalence is on the rise year by year. Vascular aging is an independent risk factor for cardiovascular diseases, and endothelial cell senescence is an early event in vascular aging. Its occurrence can lead to endothelium-dependent vasodilation dysfunction, reduced vascular permeability, and the release of the senescence-associated secretory phenotype (SASP). These vascular pathological changes further damage the vascular media, leading to vascular remodeling and reduced compliance, accelerating the progression of atherosclerosis, and ultimately resulting in cardiovascular diseases such as coronary heart disease and hypertension. Recent research of the investigators has revealed that SNRK, a new member of the AMPK family of cellular energy sensors, plays a key regulatory role in vascular development. Based on this finding, the investigators propose the scientific hypothesis that SNRK responds to both physiological and pathological aging stimuli through differential mechanisms and regulates the process of endothelial cell senescence. In this study, the investigators will explore the correlation between SNRKAS and carotid vascular structure and endothelial function by measuring the levels of the SNRK upstream lncRNA (SNRKAS) in participants' peripheral blood, in conjunction with carotid ultrasound examinations. The findings will provide a solid scientific basis for elucidating new mechanisms underlying the onset and progression of vascular aging and for identifying novel therapeutic targets.