Homocysteine was first suggested as a risk to CVD in 1969. Since then, elevated
plasma homocysteine (derived from methionine) has remained a cardiovascular risk factor with no
current treatment. Homocysteine is known to stimulate NADPH oxidase, and NADPH oxidase can
be inhibited by stimulation of the Mas receptor (MasR) of the renin angiotensin system. Stimulation
of MasR is known to reduce organ fibrosis through the production of NO. However, the role that
MasR plays in homocysteine-induced vascular pathology, including endothelial dysfunction and
organ fibrosis, is not known. The aim of this thesis is to determine if high methionine diet in MasR-/- mice will worsen cardiovascular pathology.