Basic Science Review
Matrix metalloproteinases in inflammatory bowel disease: Boon or a bane?
Article first published online: 19 DEC 2006
Copyright © 2006 Crohn's & Colitis Foundation of America, Inc.
Inflammatory Bowel Diseases
Volume 13, Issue 1, pages 97–107, January 2007
How to Cite
Ravi, A., Garg, P. and Sitaraman, S. V. (2007), Matrix metalloproteinases in inflammatory bowel disease: Boon or a bane?. Inflamm Bowel Dis, 13: 97–107. doi: 10.1002/ibd.20011
- Issue published online: 19 DEC 2006
- Article first published online: 19 DEC 2006
- Manuscript Accepted: 12 SEP 2006
- Manuscript Received: 30 AUG 2006
- National Institute of Diabetes and Digestive and Kidney Diseases. Grant Number: DK06411
- Crohn's and Colitis Foundation of America Senior Research Award
- Elseivier Research Initiative Award
Matrix metalloproteinases (MMPs) are a family of Zn2+-dependent extracellular matrix (ECM) degrading endopeptidases that share common functional domains, activation mechanisms, and collectively have the capacity to degrade all types of ECM proteins. In addition to playing a central role in ECM turnover, MMPs proteolytically activate or degrade a variety of nonmatrix substrates including chemokines, cytokines, growth factors, and junctional proteins. Thus, they are increasingly recognized as critical players in inflammatory response. Indeed, accumulating data from several studies indicate that they are the predominant proteases involved in the pathogenesis of inflammatory bowel disease (IBD) via their influence on the function and migration of inflammatory cells, mucosal ulceration, as well as matrix deposition and degradation. Some MMPs are constitutively expressed and play a protective role in IBD through their effect on cellular homeostasis, while others are induced during inflammation-mediated tissue damage. This article focuses on the role of the various MMPs in IBD, discussing their physiologic and pathogenetic role in the context of intestinal defense, mucosal inflammatory response, and immune cell-epithelial interaction.
(Inflamm Bowel Dis 2007;13:97–107)