The aim of present work was to evaluate whether endoglin is co-expressed with SMAD2, phosphorylated SMAD2/3 and eNOS in endothelium of normocholesterolemic C57BL/6J mice, and in advanced atherosclerotic lesions in hypercholesterolemic apoE/LDLr-deficient mice by means of fluorescence immunohistochemistry. The results suggest that endoglin, SMAD2, phosphorylated SMAD2/3 and eNOS may be important in vessel endothelium homeostasis underlying their role in atherogenesis.