Plasminogen activator inhibitor 1 (PAI-1) plays a key role in regulating fibrinolysis, the process that breaks down blood clots. By inhibiting tissue plasminogen activator (tPA) and urokinase (uPA), PAI-1 helps control clot stability and prevents excessive bleeding. This makes it a critical target in conditions involving abnormal clot formation or breakdown, such as deep vein thrombosis, pulmonary embolism, and ischemic stroke.

In cardiovascular research, elevated levels of PAI-1 are associated with increased risk of thrombosis and atherosclerosis, making it a biomarker for assessing thrombotic risk. It is also implicated in metabolic disorders like obesity and type 2 diabetes, where high PAI-1 levels contribute to impaired fibrinolysis and increased cardiovascular complications.

PAI-1 is being studied as a therapeutic target in antifibrotic treatments. Overexpression of PAI-1 is linked to tissue fibrosis in organs such as the liver, lungs, and kidneys. Inhibiting PAI-1 activity may slow fibrotic progression and support tissue remodeling.

In cancer research, PAI-1 is involved in cell migration, invasion, and angiogenesis. Its dual role—both promoting and inhibiting tumor progression—makes it a focus in understanding metastasis and developing targeted therapies.

Due to its central role in coagulation, fibrosis, and cell mobility, PAI-1 is a significant molecule in diagnostic development and drug discovery across multiple disease areas.