Pathogenesis of chronic obstructive pulmonary disease.
The pathogenesis of chronic obstructive pulmonary disease (COPD) encompasses a number of injurious processes, including an abnormal inflammatory response in the lungs to inhaled particles and gases. Other processes, such as failure to resolve inflammation, abnormal cell repair, apoptosis, abnormal cellular maintenance programs, extracellular matrix destruction (protease/antiprotease imbalance), and oxidative stress (oxidant/antioxidant imbalance) also have a role. The inflammatory responses to the inhalation of active and passive tobacco smoke and urban and rural air pollution are modified by genetic and epigenetic factors. The subsequent chronic inflammatory responses lead to mucus hypersecretion, airway remodeling, and alveolar destruction. This article provides an update on the cellular and molecular mechanisms of these processes in the pathogenesis of COPD.
Macnee
William
W
ELEGI Colt Research Laboratories, MRC Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, 47 Little France Avenue, Edinburgh EH16 4TJ, Scotland, UK. w.macnee@ed.ac.uk
D005540:Forced Expiratory Flow Rates / Q000502:physiology; D006801:Humans; D011379:Prognosis; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000503:physiopathology; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects