Genetic variants, gene expression, and soluble CD36 analysis in acute coronary syndrome: Differential protein concentration between ST‐segment elevation myocardial infarction and unstable angina

Background Atherosclerosis plays an important role in the pathophysiology of acute coronary syndrome (ACS). CD36 is a scavenger receptor involved in lipid metabolism. Some single‐nucleotide variants in the non‐coding region could indirectly alter the expression and the function of the protein. Objective The aim of this study was to investigate the gene and protein expression associated with CD36 variants (rs1194182;C > G; rs1049654;C > A, rs1334512;G > T, and rs3211892;G > A) in ACS patients from the western Mexican population. Methods We recruited 310 ACS patients and 308 subjects in the control group (CG). Genotyping was determined by TaqMan SNP genotyping assays. CD36 expression at the mRNA level was quantified by TaqMan gene expression assays. Soluble CD36 (sCD36) was measured by enzyme‐linked immunosorbent assay. Results We show that rs1194182G > C variant provides a protective effect with a 1.7‐fold lower susceptibility to develop ACS (p = 0.03); however, this association was masked by diabetes and dyslipidemia. We observed a higher sCD36 concentration in patient with ST‐segment elevation myocardial infarction (STEMI) compared with patients with unstable angina (UA) (p = 0.038). Likewise, in diabetic patients versus non‐diabetic (p C variant provides a protective effect with a 1.7‐fold lower susceptibility to develop ACS. ACS patients presented 1.91‐fold more CD36 mRNA compared with the control group. We observed a higher sCD36 concentration in patient with STEMI compared