The overexpression of IL1B can induce the apoptosis of endothelial and smooth muscle cells, exacerbate endothelial dysfunction, and promote the differentiation of smooth muscle cells into osteoblast-like cells, thereby accelerating the process of arterial calcification.[34] TNF is a critical regulator of immune and inflammatory responses, as it can activate immune cells, induce the production of inflammatory factors, and promote cell apoptosis. Here, TNF is linked to endothelial dysfunction.