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首页> 外文期刊>Progress in Cardiovascular Diseases >Genetic influence on cigarette-induced cardiovascular disease.
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Genetic influence on cigarette-induced cardiovascular disease.

机译：遗传因素对香烟诱发的心血管疾病的影响。

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Cigarette smoking as an addictive habit has accompanied human beings for more than 4 centuries. It is also one of the most potent and prevalent environmental health risks human beings are exposed to, and it is responsible for more than 1000 deaths each day in the United States. With recent research progress, it becomes clear that cigarette smoking can cause almost all major diseases prevalent today, such as cancer or heart disease. These detrimental effects are not only present in active smokers who choose the risk, but also to innocent bystanders, as passive smokers, who are exposed to cigarettes not-by-choice. While the cigarette-induced harm to human health is indiscriminate and severe, the degree of damage also varies from individual to individual. This intersubject variability in cigarette-induced pathologies is partly mediated by genetic variants of genes that may participate in detoxification process, eg, cytochrome P450 (CYP), cellular susceptibility to toxins, such as p53, or disease development. Through population studies, we have learned that certain CYP1A1 variants, such as Mspl polymorphism, may render the carriers more susceptible to cigarette-induced lung cancer or severe coronary atherosclerosis. The endothelial nitric oxide synthase intron 4 rare allele homozygotes are more likely to have myocardial infarction if they also smoke. In vitro experimental approach has further demonstrated that cigarettes may specifically regulate these genes in genotype-dependent fashion. While we still know little about genetic basis and molecular pathways for cigarette-induced pathological changes, understanding these mechanisms will be of great value in designing strategies to further reduce smoking in targeted populations, and to implement more effective measures in prevention and treatment of cigarette-induced diseases. Copyright 2003, Elsevier Science (USA). All rights reserved.
机译：吸烟已成为一种成瘾习惯，已经伴随着人类四个多世纪了。它也是人类面临的最有力和最普遍的环境健康风险之一，在美国每天造成超过1000人死亡。随着最近的研究进展，很明显，吸烟会导致当今几乎所有流行的主要疾病，例如癌症或心脏病。这些有害影响不仅存在于选择风险的主动吸烟者中，而且还表现为无辜的旁观者，例如被动吸烟者，他们被动地接触香烟。尽管香烟对人类健康的危害是不加区别的并且是严重的，但损害程度也因人而异。香烟诱发的病理学中这种受试者间的变异性部分地由可能参与解毒过程的基因的遗传变异（例如细胞色素P450（CYP），细胞对毒素（如p53）的易感性或疾病发展）介导。通过人群研究，我们了解到某些CYP1A1变异体，例如Mspl多态性，可能使携带者更容易受到香烟诱发的肺癌或严重的冠状动脉粥样硬化的影响。内皮一氧化氮合酶内含子4个罕见的等位基因纯合子如果也抽烟，则更可能患有心肌梗塞。体外实验方法进一步证明，香烟可能以基因型依赖性的方式特异性调控这些基因。尽管我们对卷烟引起的病理变化的遗传基础和分子途径仍然知之甚少，但了解这些机制对于设计进一步减少目标人群吸烟以及实施预防和治疗卷烟的有效措施的策略具有重要价值。诱发疾病。版权所有（Elsevier Science）（美国），2003年。版权所有。

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