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

Published

Journal Article (Review)

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.

Full Text

Duke Authors

Cited Authors

  • Fischer, BM; Pavlisko, E; Voynow, JA

Published Date

  • 2011

Published In

Volume / Issue

  • 6 /

Start / End Page

  • 413 - 421

PubMed ID

  • 21857781

Pubmed Central ID

  • 21857781

Electronic International Standard Serial Number (EISSN)

  • 1178-2005

Digital Object Identifier (DOI)

  • 10.2147/COPD.S10770

Language

  • eng

Conference Location

  • New Zealand