Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Impaired fibrinolysis may be associated with development of atherothrombotic cardiovascular disease (CVD) in metabolic syndrome or type 2 diabetes. Plasma plasminogen activator inhibitor (PAI)-1, a potent inhibitor of fibrinolysis, is elevated in a number of clinical situations that are associated with high incidence of CVD. Impaired fibrinolysis resulting from high plasma PAI-1 can lead to excessive fibrin accumulation within vessels, resulting in atherothrombosis. Increased expression of PAI-1 is found in atherosclerotic lesions in humans, especially atherosclerotic plaques in patients with type 2 diabetes. This increased vascular expression of PAI-1 promotes neointima formation via accumulation of fibrin or fibrinogen as a result of inhibited clearance of platelet-fibrin thrombi. PAI-1, an acute phase protein, also could be involved in vascular inflammation. PAI-1 may be associated not only systemically but also locally with development of CVD.