Activin A a member of TGF-B superfamily has been involved in several pathologic
processes. It is also accused to have a pathognomonic role in atherogenesis and the
development of heart failure. Its activity is regulated by a glycoprotein called
follistatin that bind activin preventing its function. uPA is a serine protease that
activates plasminogen thus initiating a cascade of fibrinolysis and extra cellular
proteolysis. The aim of this study is to assess the role of activinA, follistatin and uPA
in patients with chronic heart failure and to find if there is any correlation among
their levels. The present study was conducted on 30 patients with chronic heart
failure as a result of cardiomyopathy or ischemic heart diseases (group I). There
were 20 healthy subjects of matched age and sex involved in the study as a control
group (group II). In both groups serum activin A, follistatin, uPA and lipid profile
that included serum T.G, total cholesterol, LDLc and HDLc were estimated. Results:
there was a significant increase in serum activin A and follistatin and a significant
decrease of uPA in group I as compared to controls. As regard to lipid profile there
was a significant increase in serum T.G, serum total cholesterol and serum LDLc in
group I than group II while there was a significant decrease in patients than the
controls regarding HDLc. There was significant positive correlation between activin
A and urokinase plasminogen activator (uPA) in group 1. Conclusion:activin
A/follistatin system may play a role in the pathogenesis of heart failure; also uPA
could be suggested to have an important role in atherosclerosis and ischemic
vascular disease that predisposes to heart failure due to the possible role of activin A
cytokine in the fibrinolytic activity of uPA.