In cAD, significant correlations (P < 0.001) were observed between: Cdk5/p35 and GSK3β<sub>tyr216</sub> ; a-casp3 and Aβ<sub>42</sub> ; p53 and age at death.
We evaluated possible gene polymorphisms of tumor protein 53 ( TP53, rs1042522, rs1042522;rs1131691014;rs878854066" genes_norm="7157">p.Arg72Pro) that can differentiate LM-CAD from patients with more peripheral CAD (MP-CAD) and healthy participants (control group) in 520 individuals (LM-CAD, n = 175; MP-CAD, n = 185; and control group, n = 160).
In the present study, we found that the SIRT1 expression levels were repressed and the acetylated p53 expression levels were enhanced in the monocytes of patients with CAD.
The authors have investigated the possible association of p53 codon 72 polymorphism with left ventricular ejection fraction (LVEF) in subjects with and without coronary artery disease (CAD).
The data suggest an interaction between p53 codon 72 and ACPACP₁ wherein a positive effect of the p53 *Pro allele on susceptibility to CAD occurs, but only in the presence of the ACPACP₁ genotype characterized by high enzymatic activity.
Subjects carrying both the *T allele of PTPN22 and the *Pro allele of p53 were overrepresented in CAD nondiabetic cases relative to the other two groups (p = 0.001).
Patients presenting with polymorphisms of FAS LG, FAS promoter and TP53 have an increased risk of CAD progression, as they have a higher rate of re-interventions.
Our findings identify an interactive effect of both p53 polymorphisms and cigarette smoking on the occurrence of coronary artery disease in that non-smoking patients with rare alleles at both sites had increased incidence of CAD.