Factor Seven Activating Protease » Clinical Studies

Factor VII-Activating Protease (FSAP) in atherosclerotic plaques

admin — Sun, 24 May 2009 20:18:48 +0000

FSAP was studied at the protein level (immuno-histochemistry) and the mRNA level (PCR) in atherosclerotic lesions obtained by directional coronary atheroectomy. Higher levels of FSAP mRNA (p<0,001) as well as FSAP antigen (p<0,005) were observed in patients with acute coronary syndromes compared to patients with stable angina pectoris. FSAP was also found to be co-localized with the macrophage-rich shoulder of the plaques. In vitro experiments indicated that monocyte-derived macrophages can express FSAP. Parahuleva and his colleagues concluded that FSAP may play a role in plaque destabilization.

Title:
Factor Seven Activating Protease (FSAP) expression in human monocytes and accumulation in unstable coronary atherosclerotic plaques.

Authors and Source:
Parahuleva et al. Atherosclerosis. 2008 Jan;196(1):164-171.

Factor VII-Activating Protease and Liver Cirrhosis

admin — Sun, 24 May 2009 18:05:17 +0000

Wasmuth and colleagues addressed the fact that genetic factors affect the progression of liver fibrosis in chronic hepatitis C (HCV) infection and they asked whether the Marburg I variant of FSAP (FSAP G511E allele) might play a role. Their findings suggest that the G511E variant is a risk locus for HCV-induced liver fibrosis and cirrhosis. The reason may be the reduced ability of FSAP-MI to down-regulate PDGF-mediated hepatic stellate proliferation (see Roderfeld et al. below, link). The authors conclude that FSAP G511E “… might be useful for risk stratification in patients with HCV-infection”.

Title:
The marburg I variant (G534E) of the factor VII-activating protease determines liver fibrosis in hepatitis C infection by reduced proteolysis of platelet-derived growth factor BB.

Authors and Source:
Wasmuth et al. Hepatology. 2009 Mar;49(3):775-780.