Key result
Measuring plasma PAI-1 concentration alone misleads risk assessment without evaluating its functional stability.
Answers are grounded in this paper and cite their sources.
Reviews the regulation and stability of plasminogen activator inhibitor-1, highlighting therapeutic targeting for cardiovascular disease.
Plasminogen activator inhibitor-1 (PAI-1) is the main inhibitor of plasminogen activators, such as tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA), and a major regulator of the fibrinolytic system. PAI-1 plays a pivotal role in acute thrombotic events such as deep vein thrombosis (DVT) and myocardial infarction (MI). The biological effects of PAI-1 extend far beyond thrombosis including its critical role in fibrotic disorders, atherosclerosis, renal and pulmonary fibrosis, type-2 diabetes, and cancer. The conversion of PAI-1 from the active to the latent conformation appears to be unique among serpins in that it occurs spontaneously at a relatively rapid rate. Latency transition is believed to represent a regulatory mechanism, reducing the risk of thrombosis from a prolonged antifibrinolytic action of PAI-1. Thus, relying solely on plasma concentrations of PAI-1 without assessing its function may be misleading in interpreting the role of PAI-1 in many complex diseases. Environmental conditions, interaction with other proteins, mutations, and glycosylation are the main factors that have a significant impact on the stability of the PAI-1 structure. This review provides an overview on the current knowledge on PAI-1 especially importance of PAI-1 level and stability and highlights the potential use of PAI-1 inhibitors for treating cardiovascular disease.
No takes yet. Share an insight, caveat, or question.
Yıldız et al. (2014) conducted a review in Cardiovascular disease, thrombosis, and fibrotic disorders. Plasminogen activator inhibitor-1 (PAI-1) stability and function was evaluated. Relying solely on plasma concentrations of PAI-1 without assessing its functional stability may be misleading in interpreting its role in complex diseases.
Synapse has enriched 10 related papers. Consider them for comparative context: