The pathogenesis of chronic obstructive pulmonary disease.
Cigarette smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD). An accelerated rate of lung function decline that causes clinically significant COPD, however, is present in only a minority of smokers. In addition to the cumulative amount of cigarettes smoked, other environmental and genetic properties contribute to this variable physiological response. This article reviews the role of airway hyperresponsiveness, mucus hypersecretion, infection, and proteases in the development of COPD.
Markewitz
B A
BA
Section of Pulmonary and Critical Care Medicine, Department of Medicine, Overton Brooks Veterans Administration Medical Center, Shreveport, Louisiana 71101-4295, USA.
Owens
M W
MW
Payne
D K
DK
D001980:Bronchi / Q000378:metabolism; D016535:Bronchial Hyperreactivity / Q000150:complications / Q000209:etiology; D004391:Dust / Q000009:adverse effects; D010450:Endopeptidases / Q000378:metabolism; D006801:Humans; D008173:Lung Diseases, Obstructive / Q000150:complications / Q000209:etiology* / Q000378:metabolism; D009093:Mucus / Q000378:metabolism; D016273:Occupational Exposure / Q000009:adverse effects; D016877:Oxidants / Q000378:metabolism; D011480:Protease Inhibitors / Q000378:metabolism; D012141:Respiratory Tract Infections / Q000150:complications; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
D004391:Dust; D016877:Oxidants; D011480:Protease Inhibitors; D014028:Tobacco Smoke Pollution; D010450:Endopeptidases