Abstract
RATIONALE: Fibrotic tissue remodeling is central to the pathogenesis of both airway remodeling in asthma and parenchymal remodeling in fibrotic interstitial lung disorders. Evidence from both patients and animal models implicates prostaglandin E2 (PGE2) as well as the degree of fibrinolysis, in turn dictated by the balance of urokinase plasminogen activator (uPA) and plasminogen activator inhibitor (PAI-1), as key anti-fibrotic mediators. However, little is known about the cross-talk between these two mediator systems.
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