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Am J Physiol Lung Cell Mol Physiol 283: L1-L11, 2002; doi:10.1152/ajplung.00489.2001
1040-0605/02 $5.00
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Vol. 283, Issue 1, L1-L11, July 2002

INVITED REVIEW
Metalloproteinase and growth factor interactions: do they play a role in pulmonary fibrosis?

Margaret K. Winkler1 and John L. Fowlkes2

1 Department of Pediatrics, University of Alabama at Birmingham and Children's Hospital of Alabama, Birmingham, Alabama 35233; and 2 Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital, Little Rock, Arkansas 72202

Chronic lung disease due to interstitial fibrosis can be a consequence of acute lung injury and inflammation. The inflammatory response is mediated through the migration of inflammatory cells, actions of proinflammatory cytokines, and the secretion of matrix-degrading proteinases. After the initial inflammatory insult, successful healing of the lung may occur, or alternatively, dysregulated tissue repair can result in scarring and fibrosis. On the basis of recent insights into the mechanisms underlying acute lung injury and its long-term consequences, data suggest that proteinases, such as the matrix metalloproteinases (MMPs), may not only be involved in the breakdown and remodeling that occurs during the injury but may also cause the release of growth factors and cytokines known to influence growth and differentiation of target cells within the lung. Through the release of and activation of fibrosis-promoting cytokines and growth factors such as transforming growth factor-beta 1, tumor necrosis factor-alpha , and insulin-like growth factors by MMPs, we propose that these metalloproteinases may be integral to the initiation and progression of pulmonary fibrosis.

acute respiratory distress syndrome; bronchopulmonary dysplasia; lung fibrosis; cytokines; emphysema


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