Background Chronic obstructive pulmonary disease (COPD) is a complex disorder with unexplained heritability. Interactions of genetic and environmental factors are thought to be crucial in COPD. So, we aim to examine interactions of the endothelial nitric oxide synthase (eNOS) and angiotensin converting enzyme (ACE) genes and cigarette smoking in COPD. Methods The eNOS G 894T and ACE ID variants were analyzed in 122 COPD patients and 200 controls from Serbia. The effect of the variants on COPD was assessed by logistic regression. Interactions between eNOS, ACE and cigarette smoking in COPD were evaluated using a case-control model. Interaction between the genes was analyzed in silico. Results No effect of the eNOS G 894T and ACE ID variants on COPD was found in our study. Gene-gene interaction between the eN OS T T and A CE D was identified (p=0.033) in COPD. The interaction is realized within the complex network of biochemical pathways. Gene-environment interactions between the eNOS T and cigarette smoking (p=0.013), and the ACE II and cigarette smoking (p=0.009) were detected in COPD in our study. Conclusions This is the first research to reveal interactions of the eNOS and ACE genes and cigarette smoking in COPD progressing our understanding of COPD heritability and contributing to the development of appropriate treatments.

中文翻译：

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eNOS 和 ACE 基因与吸烟在慢性阻塞性肺病中的相互作用。

背景 慢性阻塞性肺疾病 (COPD) 是一种具有无法解释的遗传性的复杂疾病。遗传和环境因素的相互作用被认为在 COPD 中至关重要。因此，我们的目标是检查内皮一氧化氮合酶 (eNOS) 和血管紧张素转换酶 (ACE) 基因与吸烟在 COPD 中的相互作用。方法 在来自塞尔维亚的 122 名 COPD 患者和 200 名对照者中分析了 eNOS G 894T 和 ACE ID 变体。通过逻辑回归评估变体对 COPD 的影响。使用病例对照模型评估 COPD 中 eNOS、ACE 和吸烟之间的相互作用。在计算机上分析了基因之间的相互作用。结果 在我们的研究中未发现 eNOS G 894T 和 ACE ID 变体对 COPD 有影响。鉴定了 eN OS TT 和 A CE D 之间的基因-基因相互作用 (p=0. 033) 在慢性阻塞性肺病中。这种相互作用是在生化途径的复杂网络中实现的。在我们的研究中，在 COPD 中检测到 eNOS T 与吸烟 (p=0.013) 以及 ACE II 与吸烟 (p=0.009) 之间的基因-环境相互作用。结论 这是首次揭示 eNOS 和 ACE 基因与吸烟在 COPD 中相互作用的研究，加深了我们对 COPD 遗传性的理解，并有助于开发适当的治疗方法。