This often involves telomere shortening, accrual of DNA damage, and progressive mitochondrial dysfunction, which leads to increased reactive oxygen species and decreased nitric oxide production and increased p53, p16, and p21 expression and activation, ultimately culminating in impaired endothelium vasodilation, increased thrombogenesis, accelerated atherosclerosis, and reduced angiogenesis (47). Here, TP53 is linked to atherosclerosis.