Matrix Metalloproteinases and TIMPs: Properties and Implications for the Treatment of Chronic Obstructive Pulmonary Disease

  1. Derek Chadwick Organizer and
  2. Jamie A. Goode
  1. Tim Cawston,
  2. Severine Carrere,
  3. Jon Catterall,
  4. Richard Duggleby,
  5. Sarah Elliott,
  6. Bill Shingleton and
  7. Andrew Rowan

Published Online: 7 OCT 2008

DOI: 10.1002/0470868678.ch13

Chronic Obstructive Pulmonary Disease: Pathogenesis to Treatment: Novartis Foundation Symposium 234

Chronic Obstructive Pulmonary Disease: Pathogenesis to Treatment: Novartis Foundation Symposium 234

How to Cite

Cawston, T., Carrere, S., Catterall, J., Duggleby, R., Elliott, S., Shingleton, B. and Rowan, A. (2000) Matrix Metalloproteinases and TIMPs: Properties and Implications for the Treatment of Chronic Obstructive Pulmonary Disease, in Chronic Obstructive Pulmonary Disease: Pathogenesis to Treatment: Novartis Foundation Symposium 234 (eds D. Chadwick and J. A. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/0470868678.ch13

Author Information

  1. Department of Rheumatology, Department of Medicine, University of Newcastle, Framlington Place, Newcastle upon Tyne NE2 4HH, UK

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 28 NOV 2000

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780471494379

Online ISBN: 9780470868676

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Summary

The matrix metalloproteinases (MMPs) are a unique family of metalloenzymes that, once activated, can destroy connective tissue. The active enzymes are all inhibited by tissue inhibitors of metalloproteinases (TIMPs). The relative amounts of active MMPs and TIMPs are important in determining whether tissues are broken down in disease. Although elastase is often regarded as the target enzyme in chronic obstructive pulmonary disease (COPD), both the neutrophils and macrophages in the lung contain metalloproteinases and both collagen and elastin are degraded in disease. Transgenic studies have shown that when MMP1 is over-expressed, pulmonary emphysema develops in mice, while MMP12 knockout mice do not develop pulmonary emphysema when exposed to cigarette smoke. New drugs that can specifically block active MMPs are now available. These potent inhibitors are effective in vitro and prevent the destruction of tissue in animal models. Future patient trials will test the effectiveness of these compounds in preventing tissue destruction.