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Pathogenic triad in COPD: oxidative stress, protease–antiprotease imbalance, and inflammation

Authors Fischer BM, Pavlisko E, Voynow JA

Published Date August 2011 Volume 2011:6 Pages 413—421

DOI http://dx.doi.org/10.2147/COPD.S10770

Published 5 August 2011

Bernard M Fischer1, Elizabeth Pavlisko2, Judith A Voynow1
1Department of Pediatrics, 2Department of Pathology, Duke University Medical Center, Durham, NC, USA

Abstract: 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.

Keywords: senescence, apoptosis, chronic obstructive pulmonary disease, bronchitis, emphysema

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