Nagai Atsushi
First Department of Medicine, Tokyo Women's Medical University School of Medicine.
Nihon Rinsho. 2003 Dec;61(12):2126-32.
Although the major sites of airflow limitation in patients with COPD are most likely the peripheral airways, lesions in both the peripheral airways and the lung parenchyma contribute to chronic airflow limitations. Abnormalities in the lung parenchyma is recognized as emphysema characterized by air space enlargement and alveolar destruction. The mechanism responsible for the development of emphysema was thought to be protease/antiprotease imbalance and oxidative stress. A very recent study shows that alveolar cell apoptosis causes lung destruction and emphysematous changes. Thus, apoptosis may play a significant role in the development of emphysema.
虽然慢性阻塞性肺疾病(COPD)患者气流受限的主要部位很可能是外周气道,但外周气道和肺实质的病变均会导致慢性气流受限。肺实质异常表现为以气腔扩大和肺泡破坏为特征的肺气肿。肺气肿发生的机制曾被认为是蛋白酶/抗蛋白酶失衡和氧化应激。最近的一项研究表明,肺泡细胞凋亡会导致肺组织破坏和肺气肿改变。因此,细胞凋亡可能在肺气肿的发生发展中起重要作用。