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The FASEB Journal, Vol 8, 854-861, Copyright © 1994 by The Federation of American Societies for Experimental Biology
REVIEWS |
EJ Kovacs and LA DiPietro
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Stritch School of Medicine, Maywood, Illinois 60153.
The pathogenesis of fibrotic disorders is similar regardless of the tissues involved. Inflammatory leukocytes infiltrate the site triggered by chemotactic and activating mediators. This is followed by the elaboration of cytokines that directly and indirectly induce the proliferation of fibroblasts and endothelial cells and the deposition of extracellular matrix (ECM). In the absence of inhibitory signals, the continued production of these mediators sustains the connective tissue accumulation, which results in permanent alteration in tissue structure and function.
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