Pathogenic triad in COPD: oxidative stress, protease-antiprotease imbalance, and inflammation.
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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.
chronic obstructive pulmonary disease
Genome-Wide Association Study
Pulmonary Disease, Chronic Obstructive
Reactive Oxygen Species
Respiratory Function Tests
Published Version (Please cite this version)10.2147/COPD.S10770
Publication InfoFischer, Bernard Martin; Pavlisko, Elizabeth N; & Voynow, JA (2011). Pathogenic triad in COPD: oxidative stress, protease-antiprotease imbalance, and inflammation. Int J Chron Obstruct Pulmon Dis, 6. pp. 413-421. 10.2147/COPD.S10770. Retrieved from https://hdl.handle.net/10161/13743.
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Associate Professor of Pediatrics
Comparative Pharmacology and Cell Biology Mechanisms of complementary-alternative medicines and products Signal Transduction and Cell Signaling Development of both animal and in vitro models of disease Implications of early life lung injury on long-term immune function and overall health Mechanisms of inflammation and disease Cytokine, Oxidant, and Inflammatory Mediator NetworkingIntegrative care/treatments for HIV patientsMechanisms of chronic inf
Assistant Professor of Pathology
Dr. Pavlisko joined the faculty in 2011 as an Assistant Professor of Pathology at Duke University Medical Center where her work is focused in thoracic, cardiovascular and transplant pathology as well as postmortem examination. She is the co-author of the chapter Mesothelioma in the 3rd edition of Pathology of Asbestos-Associated Diseases, the chapter Lung Cancer in the new text titled Occupational Cancer (both of which were published in 2014), and the chapter Diseases of Se
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