Sharafkhaneh Amir, Hanania Nicola A, Kim Victor
Division of Pulmonary, Critical Care and Sleep Medicine, Baylor College of Medicine, Houston, TX 77030, USA.
Proc Am Thorac Soc. 2008 May 1;5(4):475-7. doi: 10.1513/pats.200708-126ET.
Chronic obstructive pulmonary disease (COPD) is characterized physiologically by expiratory flow limitation and pathologically by alveolar destruction and enlargement and small and large airway inflammation and remodeling. An imbalance between protease and antiprotease activity in the lung is proposed as the major mechanism resulting in emphysema. The imbalance is mostly due to an increase in the numbers of alveolar macrophages and neutrophils. Emphysema can also develop from increased alveolar wall cell death and/or failure in alveolar wall maintenance. Chronic inflammation and increased oxidative stress contribute to increased destruction and/or impaired lung maintenance and repair. Genetic factors may play an important role in disease susceptibility because only a minority of smokers develops emphysema. Recent literature implicates surfactant instability, malnutrition, and alveolar cell apoptosis as possible etiologies. Identification of cellular and molecular mechanisms of COPD pathogenesis is an area of active, ongoing research that may help to determine therapeutic targets for emphysema.
慢性阻塞性肺疾病（COPD）的生理特征是呼气气流受限，病理特征是肺泡破坏与扩大以及大小气道炎症和重塑。肺内蛋白酶和抗蛋白酶活性失衡被认为是导致肺气肿的主要机制。这种失衡主要是由于肺泡巨噬细胞和中性粒细胞数量增加。肺气肿也可因肺泡壁细胞死亡增加和/或肺泡壁维持功能障碍而发展。慢性炎症和氧化应激增加导致破坏增加和/或肺维持与修复受损。遗传因素可能在疾病易感性中起重要作用，因为只有少数吸烟者会发展为肺气肿。最近的文献表明表面活性剂不稳定、营养不良和肺泡细胞凋亡可能是病因。确定COPD发病机制的细胞和分子机制是一个正在积极进行研究的领域，这可能有助于确定肺气肿的治疗靶点。
