STAT4 rs3024839 C allele was associated with a 2.94-fold increased risk and IL22 rs2227483 T allele with a 2.56-fold increased risk of myocardial infarction in Middle Eastern adults.
Case-Control (n=800)
Yes
Do the STAT4 rs3024839 and IL22 rs2227483 polymorphisms increase the risk of myocardial infarction?
The STAT4 rs3024839 and IL22 rs2227483 polymorphisms are significantly associated with an increased risk of myocardial infarction and may serve as genetic markers for early risk prediction.
Effect estimate: OR 2.94 for STAT4 rs3024839 C allele; OR 2.56 for IL22 rs2227483 T allele (95% CI 95% CI 2.94 OR not stated for STAT4; 95% CI 2.56 OR not stated for IL22)
p-value: p=0.004 for STAT4; p<0.001 for IL22
Long-term primary prevention of myocardial infarction faces challenges, but genetic risk assessment may change this dynamic. We sought for genetic risk loci influencing myocardial infarction and underlying pathomechanisms. AS-PCR used for mutation detection (STAT4_ rs3024839 and IL22_ rs2227483) and confirmed positives by sequencing and Digital PCR. STAT4 and IL22 mRNA levels and chromatin accessibility at SNP sites were evaluated. We assessed SNPs for association with myocardial underlying comorbidities as well as their predictive performance ability. The population flow-sorted CD4+ FOXP3+ Tregs and the level of Foxp3 mRNA were measured and TGF-β1 quantified using ELISA and intracellular staining assay. Immunophenotyping used to identify p53 expression, pro-inflammatory monocytes and circulating endothelial cells. More than 99% samples were positive for mutations. Significant differences in the mutated allele and genotype frequencies were identified at a p value cutoff of 0. 05. Analyses identified SNPs as risk factors for comorbid factors with the ability in distinguishing high and low-risk individuals (AUC > 0. 9). Differentially accessible chromatin regions influencing STAT4 and IL22 expression were found in risk loci. Lower circulating CD4+ FOXP3+Tregs, Foxp3 expression decline, decreasing TGF-β1 level, increased p53 level, inflammatory state and endothelial dysfunction were further validated. Discovered genotypes open novel opportunities for MI prediction.
Nezhad et al. (Sat,) conducted a case-control in Middle Eastern adults hospitalized with first myocardial infarction without prior cardiovascular disease, matched with healthy controls (n=800). Genotyping for STAT4 rs3024839 and IL22 rs2227483 polymorphisms vs. Age- and gender-matched healthy controls without cardiovascular or chronic disease was evaluated on Association of polymorphisms rs3024839 in STAT4 and rs2227483 in IL22 with myocardial infarction occurrence (OR 2.94 for STAT4 rs3024839 C allele; OR 2.56 for IL22 rs2227483 T allele, 95% CI 95% CI 2.94 OR not stated for STAT4; 95% CI 2.56 OR not stated for IL22, p=p=0.004 for STAT4; p<0.001 for IL22). STAT4 rs3024839 C allele was associated with a 2.94-fold increased risk and IL22 rs2227483 T allele with a 2.56-fold increased risk of myocardial infarction in Middle Eastern adults.
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