Pathogenic triad in COPD: oxidative stress, protease-antiprotease imbalance, and inflammation.
Pathogenic triad in COPD: oxidative stress, protease-antiprotease imbalance, and inflammation.
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DOI：
10.2147/copd.s10770
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发表时间：
2011
影响因子：
2.8
通讯作者：
Voynow JA
中科院分区：
文献类型：
--
作者：
Fischer BM;Pavlisko E;Voynow JA
慢性阻塞性肺疾病 (COPD) 患者表现出慢性支气管炎、肺气肿和/或哮喘的主要特征，并具有气流阻塞的常见表型。 COPD肺生理学反映了COPD病理改变的总和，可发生在大中央气道、小周围气道和肺实质。定量或高分辨率计算机断层扫描用作评估疾病进展的替代措施。据报道，不同的生物或分子标记反映了炎症、蛋白酶和氧化剂的机制或致病三联体，并对应于 COPD 组织病理学的不同方面。与致病性三联体标记类似，遗传变异或多态性也与慢性阻塞性肺病相关炎症、蛋白酶-抗蛋白酶失衡和氧化应激有关。此外，近年来，有报道指出，与衰老相关的机制标记物是慢性阻塞性肺病患者肺部致病三联征的下游后果。在这篇综述中，作者将讨论仅限于对机制标记和遗传变异及其与慢性阻塞性肺病组织病理学和疾病状态的关联的综述。
Patients with chronic obstructive pulmonary disease (COPD) exhibit dominant features of chronic bronchitis, emphysema, and/or asthma, with a common phenotype of airflow obstruction. COPD pulmonary physiology reflects the sum of pathological changes in COPD, which can occur in large central airways, small peripheral airways, and the lung parenchyma. Quantitative or high-resolution computed tomography is used as a surrogate measure for assessment of disease progression. Different biological or molecular markers have been reported that reflect the mechanistic or pathogenic triad of inflammation, proteases, and oxidants and correspond to the different aspects of COPD histopathology. Similar to the pathogenic triad markers, genetic variations or polymorphisms have also been linked to COPD-associated inflammation, protease–antiprotease imbalance, and oxidative stress. Furthermore, in recent years, there have been reports identifying aging-associated mechanistic markers as downstream consequences of the pathogenic triad in the lungs from COPD patients. For this review, the authors have limited their discussion to a review of mechanistic markers and genetic variations and their association with COPD histopathology and disease status.