Hyaluronan-binding protein 2 (Factor VII-activating protease) (FSAP)

Factor VII-activating protease (FSAP), also known as Hyaluronan-binding protein 2 (HABP2), is a circulating serine protease primarily synthesized in the liver (UniProt Q14520). It plays a unique dual role in hemostasis by activating Factor VII to initiate coagulation and activating pro-urokinase to promote fibrinolysis (PMID: 11090068, 10446193). Beyond its role in blood clotting, FSAP is involved in vascular remodeling, inflammation, and tissue repair by interacting with various extracellular matrix components and cell surface receptors (PMID: 18326545). Clinical interest in FSAP is driven by its association with cardiovascular diseases, where the Marburg I polymorphism (G534E) leads to reduced enzymatic activity and an increased risk of carotid stenosis and stroke (PMID: 12446571). As a therapeutic target, modulating FSAP activity offers potential in treating thrombotic disorders and fibroproliferative diseases, though its complex regulatory network requires careful navigation to avoid adverse hemostatic effects. FSAP also exhibits inhibitory effects on vascular smooth muscle cell migration and proliferation, suggesting a protective role against atherosclerosis (PMID: 15153519).

Other names

HABP2Plasma hyaluronan-binding proteinPHBPFactor VII-activating protease

FSAP acts as a serine protease that proteolytically cleaves the zymogen Factor VII into its active form Factor VIIa, and converts pro-urokinase-type plasminogen activator (pro-uPA) into active uPA (PMID: 11090068, 10446193). It also degrades fibrinogen and inhibits vascular smooth muscle cell proliferation (PMID: 15153519).