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The plasminogen activation system in lung disease.
1Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Health Sciences Center, Ann Arbor, MI 48109-0642, USA.
Current Drug Targets
|September 28, 2007
Summary
The plasminogen activator (PA) system influences lung fibrosis. Enhancing PA activity reduces scarring, but its role in lung disease is complex, involving PAI-1.
Area of Science:
- Pulmonary Medicine
- Biochemistry
- Cell Biology
Background:
- The pulmonary alveolar space is typically pro-fibrinolytic, a state often reduced in lung diseases.
- Animal studies show manipulating the plasminogen activator (PA) system impacts lung injury fibrosis.
- Enhanced PA activity consistently reduced scarring in lung damage models.
Purpose of the Study:
- To explore the complex role of the PA system in pulmonary disorders.
- To investigate mechanisms of PA system involvement beyond simple fibrinolysis.
- To identify PAI-1 as a key target for treating lung fibrosis.
Main Methods:
- Analysis of PA system components in pulmonary disorders.
- Animal models of lung injury and fibrosis.
- Investigation of fibrinolysis and other matrix protein degradation pathways.
- Assessment of protease cascade activation, growth factor release, and cell adhesion modulation.
Main Results:
- Early findings suggested fibrin clearance by PA system reduces lung fibrosis.
- Subsequent research revealed more complex roles for the PA system.
- The serpin plasminogen activator inhibitor-1 (PAI-1) is central to these processes.
Conclusions:
- The PA system's role in lung disease is multifaceted, extending beyond fibrinolysis.
- PAI-1 is a critical regulator in lung processes, including fibrosis.
- PAI-1 represents a promising therapeutic target for lung diseases, especially fibrosis.
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