Role of the CDKN1A/p21, CDKN1C/p57, and CDKN2A/p16 Genes in the Risk of Atherosclerosis and Myocardial Infarction

p57KIP2: “Kip”ing the Cell under Control

“…The expression of p57 KIP2 is increased, whereas p21 CIP1/WAF1 and p27 KIP1 decline in both acute and end-stage heart failure, reversing to the fetal pattern of expression (198). A microsatellite polymorphism, GTn repeat, positioned in the promoter region of p57 KIP2 is related with atherosclerosis and myocardial infarction (199). The presence of the lower repeats was significantly more frequent among healthy individuals.…”

p19ARFDeficiency Reduces Macrophage and Vascular Smooth Muscle Cell Apoptosis and Aggravates Atherosclerosis

“…By analyzing a small cohort that included 316 patients and 434 controls, Rodriguez et al (18) reported lack of association between the risk of suffering myocardial infarction and the single nucleotide polymorphisms (SNPs) rs3731238, rs3814960, and rs3731249 located in the CDKN2A gene. However, recent independent genome-wide association studies that included thousands of controls and patients have identified a number of SNPs located in a region of chromosome 9p21 very close to the CDKN2A gene that are linked to high risk of atherosclerosis and associated cardiovascular disease, including coronary artery disease, myocardial infarction, and ischemic stroke (19 -25).…”

Novel Genetic Mechanisms for Aortic Aneurysms

“…Cultured SMCs from the aortae of homozygous deletion mice proliferated about twice as fast as those from controls of the same strain and did not show signs of senescence [35••]. A hyperproliferative vascular SMC phenotype is consistent with risk for atherosclerosis [36,37] and possibly occlusive disease, but the mechanism by which it contributes to aneurysms, which are characterized by SMC apoptosis and loss rather than proliferation, requires further study.…”