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 genetargeted 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.

Keywords:
COPD, chronic obstructive pulmonary disease, ECM, extracellular matrix, MMP, matrix metalloproteinase, NE, neutrophil elastase, TIMP, tissue inhibitor of metalloproteinases, COPD, emphysema, macrophage, macrophage elastase (MMP-12), neutrophil elastase
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© 2002 Biochemical Society
2002
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