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Disorders of lung matrix remodeling
Harold A. Chapman
Harold A. Chapman
Published January 15, 2004
Citation Information: J Clin Invest. 2004;113(2):148-157. https://doi.org/10.1172/JCI20729.
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Science in Medicine

Disorders of lung matrix remodeling

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Abstract

A set of lung diseases share the tendency for the development of progressive fibrosis ultimately leading to respiratory failure. This review examines the common pathogenetic features of these disorders in light of recent observations in both humans and animal models of disease, which reveal important pathways of lung matrix remodeling.

Authors

Harold A. Chapman

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Figure 2

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Determinants of lung response to breakdown in epithelial barrier functio...
Determinants of lung response to breakdown in epithelial barrier function. (a) Coordinated processes of tissue factor/factor VII complexes initiating thrombin formation and plasminogen activation by urokinase (uPA). Plasmin facilitates initial exudate turnover. Ingrowth of fibroblasts and organization of exudates into a collagenous matrix occurs quickly. (b) Maintenance of epithelial integrity, resorption of ECMs by AMs, and fibroblast apoptosis favor resolution. (c) Epithelial cell apoptosis, activation of receptors of the profibrotic cytokines thrombin, leukotrienes, and TGF-β1, and persistence of the ECM secondary to excess protease inhibitors (PAI-1 and tissue inhibitor of metalloprotease) with accumulation of fibroblast growth factors (IGF, PDGF, CTGF) favors fibrosis.
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