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首页> 外文期刊>Cytokine >Role of inflammatory gene polymorphisms in left ventricular dysfunction (LVD) susceptibility in coronary artery disease (CAD) patients
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Role of inflammatory gene polymorphisms in left ventricular dysfunction (LVD) susceptibility in coronary artery disease (CAD) patients

机译：炎症基因多态性在冠心病（CAD）患者左心功能不全（LVD）易感性中的作用

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Rationale: Inflammation exacerbates a number of deleterious effects on the heart, most notable being left ventricular dysfunction (LVD). A promoter polymorphism of the NFKB1 gene (encodes p50 subunit) results in lower protein levels of NFkB p50 subunits, which in its dimmer (p50)2 form has anti-inflammatory effects. The active NFkB transcription factor promotes the expression of over 150 target genes including IL6 and TNF-??. Therefore, the aim of the present study was to assess the association of NFKB1, IL6 and TNF-?? gene polymorphisms with LVD in coronary artery disease (CAD) patients. Methods and Results: The present study included a total of 830 subjects (600 CAD patients and 230 controls) and was carried out in two (primary and replication) cohorts. CAD patients with reduced left ventricle ejection fraction (LVEF ??45%) were categorized having LVD. The NFKB1 -94 ATTG ins/del (rs28362491), IL6 -174 G/C (rs1800795) and TNF-?? -308 G/A (rs1800629) polymorphisms were genotyped by PCR/ARMS-PCR methods. The results of the primary cohort were validated in a replicative cohort and pooled by meta-analysis using Fisher's and Mantel-Haenszel test. The analysis showed that NFKB1 ATTG1/ATTG1 genotype was significantly associated with LVD (Fisher's method p-value=0.007, Mantel-Haenszel OR=2.34), LV end diastole (p-value=0.013), end systole (p-value=0.011) dimensions, LV mass (p-value=0.024), mean LVEF (p-value=0.001) and myocardial infarction (p-value=0.043). Conclusion: Our data suggests that NFKB1 -94 ATTG ins/del polymorphism plays significant role in conferring susceptibility of LVD and ATTG1/ATTG1 genotype may modulate risk of heart failure by increasing ventricular remodeling and worsening LV function. ? 2013 Elsevier Ltd.
机译：基本原理：炎症会加重对心脏的多种有害影响，最明显的是左心功能不全（LVD）。 NFKB1基因的启动子多态性（编码p50亚基）导致NFkB p50亚基的蛋白含量降低，以二聚体（p50）2形式具有抗炎作用。活性NFkB转录因子促进包括IL6和TNF-α在内的150多个靶基因的表达。因此，本研究的目的是评估NFKB1，IL6和TNF-α的关联。冠心病（CAD）患者的LVD基因多态性。方法和结果：本研究共包括830名受试者（600名CAD患者和230名对照），并在两个（主要和复制）队列中进行。左心室射血分数降低（LVEF≥45％）的CAD患者被分类为LVD。 NFKB1 -94 ATTG ins / del（rs28362491），IL6 -174 G / C（rs1800795）和TNF-α通过PCR / ARMS-PCR方法对-308 G / A（rs1800629）多态性进行基因分型。主要队列的结果在复制队列中得到验证，并使用Fisher和Mantel-Haenszel检验通过荟萃分析汇总。分析显示NFKB1 ATTG1 / ATTG1基因型与LVD（Fisher方法p值= 0.007，Mantel-Haenszel OR = 2.34），LV舒张末期（p值= 0.013），收缩末期（p值= 0.011）显着相关）尺寸，LV质量（p值= 0.024），平均LVEF（p值= 0.001）和心肌梗塞（p值= 0.043）。结论：我们的数据表明，NFKB1 -94 ATTG ins / del多态性在赋予LVD敏感性中起着重要作用，而ATTG1 / ATTG1基因型可能通过增加心室重构和恶化LV功能来调节心力衰竭的风险。 ？ 2013爱思唯尔有限公司

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