Implications of CD36 Gene Variants in Oxidative Stress Markers Between Mexican Patients with Type 2 Diabetes and ST-Segment Elevation Myocardial Infarction

Type 2 diabetes mellitus (T2DM) affects 90% of diabetes cases and worsens cardiovascular health by causing oxidative stress, which leads to oxidized LDL (oxLDL) and foam cell formation, contributing to atherosclerosis. This study examined the relationship between <i>CD36</i> gene variants, soluble CD36 (sCD36), oxLDL, and MDA-LDL in T2DM and ST-segment elevation myocardial infarction (STE-T2DM) patients in western Mexico. The analysis included 400 T2DM patients, 400 STE-T2DM patients, and 400 healthy controls. Results showed that STE-T2DM patients were older, mainly male, and had higher rates of smoking, sedentarism, and hypertension. Both diabetic groups exhibited elevated triacylglycerols and low HDL, with significantly higher C-reactive protein in STE-T2DM (<i>p</i> < 0.0001). No significant differences in <i>CD36</i> gene variant frequencies were found, but sCD36 levels were elevated in STE-T2DM, with associations to specific genotypes. oxLDL was higher in STE-T2DM compared to controls (<i>p</i> = 0.0268). Binary logistic regression analysis identified male sex, younger age, sedentarism, and rs3173798 T/T genotype as independent risk factors for myocardial infarction (AUC: 0.9267, <i>p</i> < 0.0001). Elevated sCD36 levels may reflect atherosclerosis progression in diabetes, indicating the need for further studies to clarify CD36's role in cardiometabolic dysfunction. These findings highlight CD36's involvement in oxidative stress responses through its interaction with oxLDL and MDA-LDL, suggesting its potential role as a molecular target in antioxidant defense mechanisms.