Tatsumi Koichiro
Department of Respirology, Graduate School of Medicine, Chiba University.
Nihon Rinsho. 2007 Apr;65(4):605-10.
Cigarette smoking is the major risk factor for COPD. However, it is likely that there are important interactions between environmental factors, such as cigarette smoking, and a genetic predisposition to COPD. Single cigarette smoking causes acute reversible airway inflammation in everyone, and only 15 % of chronic smokers may develop chronic irreversible airway inflammation, resulting in the development of COPD. Fifteen percent reason has been undefined. Multiple factors may involve the pathogenesis of COPD. Cigarette smoke may upregulate the pathways linked to lung destruction and airway inflammation, such as protease and oxidative stress, and may downregulate the pathways related to the defensive mechanism, such as antiprotease and antioxidant. Other than protease-antiprotease and oxidant-antioxidant mechanisms, multiple exposures to cigarette smoke move cells into an irreversible state of senescence, or the inability to repair lung injury. Chronic exposure to smoking may affect the VEGF signaling, resulting in apoptosis of lung cell, which may partly contribute to the pathogenesis of COPD.
吸烟是慢性阻塞性肺疾病（COPD）的主要危险因素。然而，诸如吸烟等环境因素与COPD的遗传易感性之间可能存在重要的相互作用。单次吸烟会导致每个人出现急性可逆性气道炎症，而只有15%的慢性吸烟者可能会发展为慢性不可逆性气道炎症，进而导致COPD的发生。这15%的原因尚不清楚。多种因素可能参与了COPD的发病机制。香烟烟雾可能会上调与肺破坏和气道炎症相关的途径，如蛋白酶和氧化应激，并且可能下调与防御机制相关的途径，如抗蛋白酶和抗氧化剂。除了蛋白酶-抗蛋白酶和氧化剂-抗氧化剂机制外，多次接触香烟烟雾会使细胞进入不可逆的衰老状态，即无法修复肺损伤。长期接触吸烟可能会影响血管内皮生长因子（VEGF）信号传导，导致肺细胞凋亡，这可能部分促成了COPD的发病机制。
