Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Amino Acid Sequence
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Animals
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Chemotaxis, Leukocyte
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Connective Tissue / metabolism*
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Connective Tissue / pathology*
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Cytokines / biosynthesis
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Cytokines / physiology*
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Extracellular Matrix / pathology
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Extracellular Matrix / physiology
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Fibroblasts / cytology
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Fibroblasts / pathology
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Fibrosis / physiopathology*
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Humans
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Inflammation / physiopathology
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Macrophages / physiology
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Models, Biological
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Molecular Sequence Data
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Neovascularization, Pathologic
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Pulmonary Fibrosis / pathology
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Pulmonary Fibrosis / physiopathology