Key result
IL37 polymorphisms show no significant single-variant association with dilated cardiomyopathy after multiple-testing correction.
Why the study?
Dilated cardiomyopathy involves genetic and immune-inflammatory mechanisms, but the contribution of IL37 genetic variation to disease susceptibility and biochemical phenotypes remained unclear.
Are IL37 polymorphisms (rs3811045, rs3811048, rs528949769) and their haplotypes associated with dilated cardiomyopathy susceptibility and biochemical phenotypes?
Case-Control (n=90)
Are IL37 polymorphisms (rs3811045, rs3811048, rs528949769) and their haplotypes associated with dilated cardiomyopathy susceptibility and biochemical phenotypes?
Individual IL37 polymorphisms and biochemical correlates showed no significant association with dilated cardiomyopathy after multiple-testing correction, though overall haplotype distribution differed globally and warrants validation in larger cohorts.
IL37 variants should not inform DCM risk assessment; leaves open haplotype effects for replication in larger cohorts.
Dilated cardiomyopathy (DCM) is a heterogeneous myocardial disorder involving genetic and immune-inflammatory mechanisms. The contribution of IL37 genetic variation to DCM remains unclear. This study aimed to investigate associations of IL37 rs3811045, rs3811048, and rs528949769 polymorphisms and their haplotypes with DCM susceptibility and biochemical phenotypes. This case-control study included 60 patients with DCM and 30 healthy controls. The polymorphisms were genotyped by conventional PCR followed by Sanger sequencing. Genetic associations. genotype–phenotype relationships, and haplotypes were analyzed. rs3811045 and rs528949769 showed no significant independent association with DCM.The rs3811048 recessive-model association was nominal (OR = 2.750, 95% CI = 1.059–7.142; p = 0.035), but was not significant after FDR correction (q = 0.210) or adjustment for age and sex (aOR = 2.580, 95% CI = 0.968–6.880; p = 0.058). Serum creatinine differed nominally across rs3811045 (p = 0.017) and rs3811048 (p = 0.002) genotypes, with within-analysis Bonferroni-adjusted pairwise differences; neither association remained significant after FDR correction across 24 biochemical tests. Overall haplotype distribution differed between patients and controls (global p = 0.008), although individual haplotypes were nonsignificant after multiple-testing correction. No single-variant susceptibility or genotype–biochemical association remained significant after FDR correction. The exploratory global haplotype association warrants further investigation and validation in larger independent cohorts. No single-variant susceptibility or genotype–biochemical association remained significant after FDR correction. The exploratory global haplotype association warrants further investigation and validation in larger independent cohorts.
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Tuama et al. (2026) conducted a case-control in Dilated cardiomyopathy (DCM) (n=90). IL37 polymorphisms (rs3811045, rs3811048, and rs528949769) and haplotypes vs. Healthy controls / reference genotypes was evaluated on Dilated cardiomyopathy (DCM) susceptibility (rs3811048 recessive-model association) (OR 2.750, 95% CI 1.059-7.142, p=0.035 (q = 0.210 after FDR correction; aOR = 2.580, 95% CI = 0.968-6.880, p = 0.058)). IL37 polymorphisms showed no significant single-variant association with DCM after FDR correction (rs3811048 OR 2.750, 95% CI 1.059-7.142, q=0.210), though global haplotypes differed (p=0.008).
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