Pathobiologic mechanisms of chronic obstructive pulmonary disease.
COPD is a worldwide public health problem that reduces the quality of life. The exact pathways by which CS and other environmental toxins produce COPD are not known. Currently, the leading candidates are (1) the protease-antiprotease hypothesis, (2) the Dutch hypothesis, (3) the British hypothesis, and the (4) autoimmunity hypothesis. Given the heterogeneity of the disease (and phenotypes), it is probably unrealistic that one pathway will fully explain COPD pathophysiology.
Department of Medicine, The UBC James Hogg Research Centre, Providence Heart and Lung Centre, University of British Columbia, Vancouver, British Columbia, Canada.
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D056704:Adaptive Immunity; D056151:Airway Remodeling; D015415:Biomarkers / Q000378:metabolism; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D018450:Disease Progression; D004646:Emphysema / Q000201:enzymology / Q000209:etiology; D055106:Genome-Wide Association Study; D006801:Humans; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000378:metabolism; D008954:Models, Biological; D009093:Mucus / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism; D010641:Phenotype; D011480:Protease Inhibitors / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000503:physiopathology; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*
D015415:Biomarkers; D018836:Inflammation Mediators; D011480:Protease Inhibitors; D003577:Cytochrome P-450 Enzyme System; D010447:Peptide Hydrolases