Encyclopedia of Behavioral Medicine

2013 Edition
| Editors: Marc D. Gellman, J. Rick Turner

Plasminogen Activator Inhibitor (PAI-1)

  • Jonathan Newman
Reference work entry
DOI: https://doi.org/10.1007/978-1-4419-1005-9_1279

Definition

The rupture of an atherosclerotic plaque is a recognized key event in acute ischemic syndromes, such as myocardial infarctions. The intravascular thrombotic response to a ruptured plaque is a complex cascade of thrombogenic (clot-forming) and thrombolytic (clot-dissolving) mechanisms. A key component of the thrombotic cascade is plasminogen activator inhibitor type 1 (PAI-1). PAI-1 inhibits the activation of plasminogen by tissue plasminogen activator (tPA) and urokinase (uPA) and, hence, inhibits clot lysis.

PAI-1 is a single-chain glycoprotein composed of nearly 380 amino acids. It is a member of the serine proteases family and is synthesized by vascular endothelium and smooth muscle cells in both normal and atherosclerotic arteries. By synthesizing molecules like PAI-1, arterial smooth muscle cells can prevent bleeding from small vascular injuries; congenital deficiencies of PAI-1 are a rare cause of abnormal bleeding.

Associations between PAI-1 and incident or recurrent...

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References and Readings

  1. Humphries, S. E., Panahloo, A., Montgomery, H. E., Green, F., & Yudkin, J. (1997). Gene-environment interaction in the determination of levels of haemostatic variables involved in thrombosis and fibrinolysis. Thrombosis and Haemostasis, 78(1), 457–461.PubMedGoogle Scholar
  2. Juhan-Vague, I., Pyke, S. D., Alessi, M. C., Jespersen, J., Haverkate, F., & Thompson, S. G. (1996). Fibrinolytic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. ECAT Study Group. European Concerted Action on Thrombosis and Disabilities. Circulation, 94(9), 2057–2063.PubMedCrossRefGoogle Scholar
  3. Lee, M. H., Vosburgh, E., Anderson, K., & McDonagh, J. (1993). Deficiency of plasma plasminogen activator inhibitor 1 results in hyperfibrinolytic bleeding. Blood, 81(9), 2357–2362.PubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, New York 2013

Authors and Affiliations

  1. 1.Columbia UniversityNew YorkUSA