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Interstitial Fibrosis and Growth Factors
Joseph A. Lasky and Arnold R. Brody
Environmental Health Perspectives
Vol. 108, Supplement 4: Occupational and Environmental Lung Diseases (Aug., 2000), pp. 751-762
Published by: The National Institute of Environmental Health Sciences
Stable URL: http://www.jstor.org/stable/3454412
Page Count: 12
You can always find the topics here!Topics: Lungs, Fibrosis, Receptors, Idiopathic pulmonary fibrosis, Fibroblasts, Messenger RNA, Pulmonary fibrosis, Collagens, Cell growth, Asbestos
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Interstitial pulmonary fibrosis (IPF) is scarring of the lung caused by a variety of inhaled agents including mineral particles, organic dusts, and oxidant gases. The disease afflicts millions of individuals worldwide, and there are no effective therapeutic approaches. A major reason for this lack of useful treatments is that few of the molecular mechanisms of disease have been defined sufficiently to design appropriate targets for therapy. Our laboratory has focused on the molecular mechanisms through which three selected peptide growth factors could play a role in the development of IPF. Hundreds of growth factors and cytokines could be involved in the complex disease process. We are studying platelet-derived growth factor because it is the most potent mesenchymal cell mitogen yet described, transforming growth factor beta because it is a powerful inducer of extracellular matrix (scar tissue) components by mesenchymal cells, and tumor necrosis factor alpha because it is a pleiotropic cytokine that we and others have shown is essential for the development of IPF in animal models. This review describes some of the evidence from studies in humans, in animal models, and in vitro, that supports the growth factor hypothesis. The use of modern molecular and transgenic technologies could elucidate those targets that will allow effective therapeutic approaches.
Environmental Health Perspectives © 2000 The National Institute of Environmental Health Sciences