Clinical Research Institute, Center for Cardiovascular Diseases, Heinz-Meise-Strasse 100, 36199 Rotenburg an der Fulda, Germany.
Biomark Med. 2009 Oct;3(5):617-53. doi: 10.2217/bmm.09.51.
Potential mechanisms and biomarkers of atherosclerosis related to cigarette smoking - a modifiable risk factor for that disease - are discussed in this article. These include smoking-associated inflammatory markers, such as leukocytes, high-sensitivity C-reactive protein, serum amyloid A, ICAM-1 and IL-6. Other reviewed markers are indicative for smoking-related impairment of arterial endothelial function (transcapillary leakage of albumin, inhibition of endogenous nitric oxide synthase activity and reduced endothelium-dependent vasodilation) or point to oxidative stress caused by various chemicals (cholesterol oxidation, autoantibodies to oxidized low-density lipoprotein, plasma levels of malondialdehyde and F(2)-isoprostanes and reduced antioxidant capacity). Smoking enhances platelet aggregability, increases blood viscosity and shifts the pro- and antithrombotic balance towards increased coagulability (e.g., fibrinogen, von Willebrand factor, ICAM-1 and P-selectin). Insulin resistance is higher in smokers compared with nonsmokers, and hemoglobin A1c is dose-dependently elevated, as is homocysteine. Smoke exposure may influence the kinetics of markers with different response to transient or chronic changes in cigarette smoking behavior.
本文讨论了与吸烟相关的动脉粥样硬化的潜在机制和生物标志物——这种疾病的一个可改变的危险因素。这些标志物包括与吸烟相关的炎症标志物，如白细胞、高敏 C 反应蛋白、血清淀粉样蛋白 A、细胞间黏附分子-1 和白细胞介素 6。其他被审查的标志物表明吸烟会损害动脉内皮功能（白蛋白经毛细血管渗漏、内源性一氧化氮合酶活性抑制和内皮依赖性血管舒张减少），或者表明各种化学物质引起的氧化应激（胆固醇氧化、氧化型低密度脂蛋白自身抗体、血浆丙二醛和 F(2)-异前列腺素水平降低以及抗氧化能力降低）。吸烟会增强血小板聚集性，增加血液黏度，并使促凝和抗凝平衡向凝血功能增强的方向移动（如纤维蛋白原、血管性血友病因子、细胞间黏附分子-1 和 P-选择素）。与不吸烟者相比，吸烟者的胰岛素抵抗更高，血红蛋白 A1c 呈剂量依赖性升高，同型半胱氨酸也是如此。吸烟暴露可能会影响对吸烟行为的短暂或慢性变化有不同反应的标志物的动力学。
