Increased type 1 plasminogen activator inhibitor gene expression in atherosclerotic human arteries.

Abstract

Decreased fibrinolytic capacity has been sug-

Carbon Monoxide-Induced Early Thrombolysis Contributes to Heme Oxygenase-1-Mediated Inhibition of Neointimal Growth after Vascular Injury in Hypercholesterolemic Mice

“…has been demonstrated in human atherosclerotic lesions of arteries [24] and failed vein grafts [25], and in neointima after vascular injury in experimental animals [26]. Over the past few years, the pathophysiological role of PAI-1 in the vascular remodeling process underlying atherosclerosis and restenosis have been extensively studied in mouse models with PAI-1 deficiency or overexpression [15][16][17][27][28][29].…”

Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease

“…Previous studies reported the correlation of PAI‐1 with multiple conventional risk factors of CHD, eg, obesity, glycemic traits, and type 2 diabetes mellitus,6 metabolic syndrome,7 as well as correlation with vessel wall thickness 8. In addition, higher PAI‐1 expression was observed in coronary artery tissues in the presence of atherogenic lesions 9, 10. These findings raise interest in whether PAI‐1 plays a role in early atherosclerosis versus acute thrombosis.…”

The effects of the overexpression of recombinant uncoupling protein 2 on proliferation, migration and plasminogen activator inhibitor 1 expression in human vascular smooth muscle cells

“…VSMCs within the intima produce various atherogenic mediators in-cluding plasminogen activator inhibitor 1 (PAI-1) [5]. This protein is the main physiological inhibitor of tissue-type plasminogen activator and is considered to be the most important inhibitor of fibrinolysis [6]. Moreover, in VSMCs, PAI-1 promotes neointimal formation after vascular injury [7,8].…”