Because these data highlight that activation of GPBAR1 in vivo resets the molecular mechanisms involved in development of endothelial dysfunction in the CCL4 model, we have then examined whether BAR501 has the ability to counteract endothelial injury in Gpbar1+/+ and Gpbar1-/- animals administered with methionine for 4 weeks. This evidence concerns the gene CCL4 and endothelial dysfunction.