Department of Clinical Medicine, Laboratory of Experimental Therapeutics/LIM-20, School of Medicine of University of Sao Paulo, Sao Paulo 01246-903, Brazil.
Rehabilitation service, Sírio-Libanês Hospital, Sao Paulo 01308-050, Brazil.
Cells. 2019 Apr 11;8(4):342. doi: 10.3390/cells8040342.
Changes in extracellular matrix (ECM) components in the lungs are associated with the progression of respiratory diseases, such as asthma, chronic obstructive pulmonary disease (COPD), and acute respiratory distress syndrome (ARDS). Experimental and clinical studies have revealed that structural changes in ECM components occur under chronic inflammatory conditions, and these changes are associated with impaired lung function. In bronchial asthma, elastic and collagen fiber remodeling, mostly in the airway walls, is associated with an increase in mucus secretion, leading to airway hyperreactivity. In COPD, changes in collagen subtypes I and III and elastin, interfere with the mechanical properties of the lungs, and are believed to play a pivotal role in decreased lung elasticity, during emphysema progression. In ARDS, interstitial edema is often accompanied by excessive deposition of fibronectin and collagen subtypes I and III, which can lead to respiratory failure in the intensive care unit. This review uses experimental models and human studies to describe how inflammatory conditions and ECM remodeling contribute to the loss of lung function in these respiratory diseases.
肺部细胞外基质（ECM）成分的变化与呼吸系统疾病的进展有关，如哮喘、慢性阻塞性肺疾病（COPD）和急性呼吸窘迫综合征（ARDS）。实验和临床研究表明，在慢性炎症条件下，ECM 成分的结构发生变化，这些变化与肺功能受损有关。在支气管哮喘中，弹性纤维和胶原纤维的重塑，主要发生在气道壁，与粘液分泌增加有关，导致气道高反应性。在 COPD 中，I 型和 III 型胶原亚型以及弹性蛋白的变化，干扰了肺的机械性能，据信在肺气肿进展过程中，肺弹性降低起着关键作用。在 ARDS 中，间质水肿常伴有纤维连接蛋白和 I 型和 III 型胶原亚型的过度沉积，这可能导致重症监护病房的呼吸衰竭。本综述使用实验模型和人体研究来描述炎症条件和 ECM 重塑如何导致这些呼吸系统疾病的肺功能丧失。
