National Health and Medical Research Council Centre of Research Excellence for Chronic Respiratory Disease, School of Medicine, University of Tasmania, 17 Liverpool Street, Private Bag 23, Hobart, Tasmania 7000, Australia.
Expert Rev Respir Med. 2013 Jun;7(3):275-88. doi: 10.1586/ers.13.26.
The authors have reviewed the current literature on airway inflammation and remodeling in smoking-related chronic obstructive pulmonary disease (COPD). Detailed data on airway remodeling in COPD are especially sparse and how these changes lead to decline in lung function is not well understood. Small airway fibrosis and obliteration are likely to be the main contributors to physiological airway dysfunction and occur earlier than any subsequent development of emphysema. One potential mechanism contributing to small airway fibrosis/obliteration and change in extracellular matrix is epithelial-mesenchymal transition. When associated with angiogenesis (so-called epithelial-mesenchymal transition type 3) it may well also be the link with the development of cancer, which is closely associated with COPD, predominantly in large airways. The authors have focused on our recent publications in these areas. Further investigations teasing out these mechanisms will help improve our understanding of key airway disease processes in COPD, which may have major therapeutic implications.
作者回顾了与吸烟相关的慢性阻塞性肺疾病（COPD）气道炎症和重塑的现有文献。关于 COPD 气道重塑的详细数据特别稀少，这些变化如何导致肺功能下降尚不清楚。小气道纤维化和闭塞很可能是导致气道生理功能障碍的主要原因，并且比随后发生的肺气肿更早出现。导致小气道纤维化/闭塞和细胞外基质改变的一个潜在机制是上皮-间充质转化。当与血管生成（所谓的上皮-间充质转化 3 型）相关时，它也可能是与癌症发展的联系，而癌症与 COPD 密切相关，主要发生在大气道。作者关注了我们在这些领域的最新出版物。进一步的研究可以深入了解 COPD 中关键的气道疾病过程，这可能具有重要的治疗意义。
