Proteinases in chronic obstructive pulmonary disease.
Chronic obstructive pulmonary disease (COPD) is a major health problem worldwide, and we have little specific therapy to offer these patients. One potential strategy to limit loss of lung function in COPD would be to inhibit matrix-degrading proteinases. Several serine proteinases and matrix metalloproteinases are expressed in association with COPD in humans. Application of gene-targeted macrophage elastase and neutrophil elastase to a mouse model of cigarette-smoke-induced emphysema has uncovered roles for these proteinases in airspace enlargement, and has identified many interactions between these proteolytic systems.
Shapiro
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SD
Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard University Medical School, Boston, MA 02115, U.S.A. sshapiro@rics.bwh.harvard.edu
D000818:Animals; D001980:Bronchi / Q000201:enzymology; D003546:Cysteine Endopeptidases / Q000378:metabolism; D010450:Endopeptidases / Q000378:metabolism*; D006801:Humans; D020782:Matrix Metalloproteinases / Q000378:metabolism; D051379:Mice; D011650:Pulmonary Alveoli / Q000201:enzymology; D029424:Pulmonary Disease, Chronic Obstructive / Q000201:enzymology* / Q000209:etiology / Q000473:pathology; D012697:Serine Endopeptidases / Q000378:metabolism
D010450:Endopeptidases; D012697:Serine Endopeptidases; D003546:Cysteine Endopeptidases; D020782:Matrix Metalloproteinases