Fig. 2

SELENOS role in the pathophysiological processes of diabetes-induced AS. In the early AS stage, SELENOS was associated with pathogenic factors for ED, including hyperglycemia, dyslipidemia, insulin resistance and obesity, though the double-sided effects and inconsistent results were shown, which requires further studies to draw the conclusion. Moreover, SELENOS could ameliorate endothelial function, reduce adhesion molecules expression and leukocytes recruitment giving rise to the reduction of foam cells formation. During the advanced atherosclerotic lesion development, SELENOS prevented VSMCs and macrophages apoptosis, reduced vascular calcification, and alleviated inflammation in macrophages and CD4 + T cells, which contributed to inhibiting the formation of unstable plaque characterized by a thinner fibrous cap, larger necrotic core, greater inflammation and more extensive vascular calcification. SELENOS Selenoprotein S, LDL-C Low-density lipoprotein cholesterol, ox-LDL-C Oxidized LDL-C, VSMCs Vascular smooth muscle cells