Abstract

To explore the role of Interkeulin-31 (IL-31) in dilated cardiomyopathy (DCM), in our study, two SNPs of IL-31, rs4758680 (C/A) and rs7977932 (C/G), were analyzed in 331 DCM patients and 493 controls in a Chinese Han population. The frequencies of C allele and CC genotype of rs4758680 were significantly increased in DCM patients (P = 0.005, P = 0.001, resp.). Compared to CC genotype of rs4758680, the A carriers (CA/AA genotypes) were the protect factors in DCM susceptibility while the frequencies of CA/AA genotypes were decreased in the dominant model for DCM group (P < 0.001, OR = 0.56, 95%CI = 0.39–0.79). Moreover, IL-31 mRNA expression level of white blood cells was increased in DCM patients (0.072 (0.044–0.144) versus 0.036 (0.020–0.052), P < 0.001). In survival analysis of 159 DCM patients, Kaplan-Meier curve revealed the correlation between CC homozygote of rs4758680 and worse prognosis for DCM group (P = 0.005). Compared to CC genotype, the CA/AA genotypes were the independent factors in both univariate (HR = 0.530, 95%CI = 0.337–0.834, P = 0.006) and multivariate analyses after age, gender, left ventricular end-diastolic diameter, and left ventricular ejection fraction adjusted (HR = 0.548, 95%CI = 0.345–0.869, P = 0.011). Thus, we concluded that IL-31 gene polymorphisms were tightly associated with DCM susceptibility and contributed to worse prognosis in DCM patients.

Highlights

  • Dilated cardiomyopathy (DCM) as a primary myocardial disease is marked by dilation of the left ventricle as well as systolic dysfunction that is with progressive functional and structural changes [1, 2]

  • It has been delineated that the gene polymorphisms of proinflammatory cytokines such as interleukin- (IL-) 6 and tumor necrosis factor-α (TNF-α) are associated with the susceptibility and prognosis of DCM or heart failure [7,8,9]

  • Inflammatory cytokines like IL-6 in conjunction with TNF-α participated in myocyte apoptosis and myofibrosis which were involved in DCM [15, 32]

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Summary

Introduction

Dilated cardiomyopathy (DCM) as a primary myocardial disease is marked by dilation of the left ventricle as well as systolic dysfunction that is with progressive functional and structural changes [1, 2]. It affects −1/2500 adults and more common in men than in women [3, 4]. Increasing evidence supports several cytokines implicated in the inflammatory, and immune responses are participating in the pathological process of DCM even congestive heart failure [7, 8]. It has been delineated that the gene polymorphisms of proinflammatory cytokines such as interleukin- (IL-) 6 and tumor necrosis factor-α (TNF-α) are associated with the susceptibility and prognosis of DCM or heart failure [7,8,9]

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