HT exerts multidimensional effects on the formation and progression of arterial plaques through two main pathways: on one hand, HT can cause abnormal thyroid hormone levels, which in turn affect plaque formation through metabolic disorders—thyroid hormones induce dyslipidemia, thereby promoting carotid intima thickening and plaque formation, and may further increase plaque risk by influencing blood pressure and glucose regulation; on the other hand, thyroid autoantibodies directly participate in plaque progression through immune regulation, inflammatory responses, and vascular remodeling (7). This evidence concerns the gene TG and metabolic disease.