Pathogenesis of chronic obstructive pulmonary disease.
Pathogenesis of chronic obstructive pulmonary disease.
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DOI：
10.1513/pats.200504-045sr
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
MacNee, William
中科院分区：
文献类型：
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作者：
MacNee, William
目前关于慢性阻塞性肺疾病发病机制的范式是慢性气流限制是由肺部吸入颗粒和气体的异常炎症反应引起的。气道炎症在易感吸烟者中表现不同，主要涉及CD8+ T淋巴细胞、中性粒细胞和巨噬细胞。研究表明，在疾病严重程度的不同阶段，周围空气中存在炎症。另外两个过程也得到了相当多的研究关注。首先是蛋白酶-抗蛋白酶失衡，这与肺气肿的发病机制有关。然而，蛋白酶负荷增加与抗蛋白酶的功能性抑制相关的假设很难证明，现在被认为是过于简单化了。第二个过程，氧化应激，在慢性阻塞性肺疾病的许多致病过程中起作用，可能是增强炎症反应的一种机制。此外，有研究认为肺气肿的发生可能与肺泡细胞凋亡有关。其机制可能与血管内皮生长因子通路和氧化应激有关。
The current paradigm for the pathogenesis of chronic obstructive pulmonary disease is that chronic airflow limitation results from an abnormal inflammatory response to inhaled particles and gases in the lung. Airspace inflammation appears to be different in susceptible smokers and involves a predominance of CD8+ T lymphocytes, neutrophils, and macrophages. Studies have characterized inflammation in the peripheral airspaces in different stages of disease severity. Two other processes have received considerable research attention. The first is a protease-antiprotease imbalance, which has been linked to the pathogenesis of emphysema. However, the hypothesis of an increased protease burden associated with functional inhibition of antiproteases has been difficult to prove and is now considered an oversimplification. The second process, oxidative stress, has a role in many of the pathogenic processes of chronic obstructive pulmonary disease and may be one mechanism that enhances the inflammatory response. In addition, it has been proposed that the development of emphysema may involve alveolar cell loss through apoptosis. This mechanism may involve the vascular endothelial growth factor pathway and oxidative stress.