The plasmin system in airway remodeling

Recent studies suggest that the plasmin system plays an active role in tissue remodeling. Plasmin degrades the extracellular matrix (ECM), either directly removing glycoproteins from ECM or by activating matrix metalloproteinases (MMPs). PAI-1 blocking MMPs may prevent ECM degradation, but inhibitin...

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Bibliographic Details
Published in:Thrombosis Research 2003, Vol.112 (1), p.1-7
Main Authors: Kucharewicz, Iwona, Kowal, Krzysztof, Buczko, Wlodzimierz, Bodzenta-Łukaszyk, Anna
Format: Article
Language:English
Subjects:
Airway remodeling
Asthma
Asthma - enzymology
Asthma - physiopathology
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Extracellular Matrix - metabolism
Fibrinolysin - metabolism
Humans
Lung - enzymology
Lung - physiopathology
Medical sciences
Plasmin system
Pneumonia - enzymology
Pneumonia - physiopathology
Regeneration - physiology
Serine Endopeptidases - metabolism
Serine Proteinase Inhibitors - metabolism
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Summary:Recent studies suggest that the plasmin system plays an active role in tissue remodeling. Plasmin degrades the extracellular matrix (ECM), either directly removing glycoproteins from ECM or by activating matrix metalloproteinases (MMPs). PAI-1 blocking MMPs may prevent ECM degradation, but inhibiting fibrinolysis leads to fibrin accumulation and fibrosis. Components of the plasmin system including tissue plasminogen activator (t-PA), urokinase plasminogen activator (u-PA), and plasminogen activator inhibitors PAI-1 and PAI-2 are synthesised by airway cells, and inflammatory mediators affect their expression. The plasmin system, in turn, actively influences the production of inflammatory mediators and growth factors, extending pathological structural changes in the airway. Modulation of the plasmin system might be a new pharmacological strategy that could inhibit the development of airway remodeling.
ISSN:0049-3848
1879-2472
DOI:10.1016/j.thromres.2003.10.011