细胞凋亡与慢性阻塞性肺疾病

Apoptosis and chronic obstructive pulmonary disease

慢性阻塞性肺疾病（chronic obstructive pulmonary disease，COPD）定义为气道的慢性炎症、肺实质进行性的破坏，大部分由抽烟引起。涉及到以下几个机制：气道的慢性炎症、蛋白酶／抗蛋白酶失衡、氧化应激。最近的文献提及COPD第4个重要的机制肺内结构细胞的凋亡，血管内皮生长因子在其中起重要作用。凋亡的途径：如caspase-3、神经酰胺等，可以作为预防凋亡和肺气肿发生的靶途径。本篇综述就COPD凋亡机制的相关文献进行讨论，为COPD和肺气肿的凋亡机制提供一些新的文献。

Chronic obstructive pulmonary disease （COPD） is defined by chronic inflammation of airway and progressive destruction of lung parenchyma,most cases are initiated by cigarette smoking. Several mechanisms are involved in the development of the disease： chronic inflammation of the airways, imbalance between proteolytic and anti-proteolytic activity and oxidative stress. Recently, an increasing number of data suggests a fourth important mechanism involved in the development of COPD：apoptosis of structural cells in the lung,and data from animal models suggest an important role for vascular endothelial growth factor in it. The mediators of apoptosis,such as caspase-3 and ceramide,could be interesting targets to prevent apoptosis and the development of emphysema. In this review,recent data on the role of apoptosis in COPD from both animal models as well as from studies on human subjects will be discussed. The aim is to provide an up-to-date summary on the increasing knowledge on the role of apoptosis in COPD and pulmonary emphysema.