The role of transforming growth factor-beta in identifying patients with coronary artery disease

Abstract

Transforming growth factor-beta (TGF-beta) is a cytokine with antiatherogenic propretis. The active form of TGF-beta inhibits the activation of endothelial cells, and acts on vascular smooth muscle cells by inhibiting their migration, dediferentiation and proliferation. Lipoprotein (a) i PAI-1 interfere with plasmin-mediated TGF-beta activation by inhibiting the conversion of plasminogen to plasmin. Genetic polymorphism in the TGF beta(1) gene promoter were shown to be correlated with total TGF-beta concentrations, as measured by ELISA after acetic acid/urea activation. Althought many patients with coronary artery disease (CAD) have total TGF-beta concentration below the detection limit, the ability of total TGF-beta assay in discriminating between patients with CAD and individuals with normal coronary arteries is rather limited. Very significant inverse relationship between the concentration of active TGF-beta and CAD was found in several retrospective studies. Minor overlapping between the values in CAD patients and controls was obtained, demostrating the potential of the active TGF-beta as a new marker of CAD, superior to any of the conventional risk factors.