Translational Nephrology

bone marrow; renin Angiotensin II (Ang II) has long been considered the ma-jor bioactive effector molecule of the renin–angiotensin system and is recognized as a major contributor to hypercholesterolaemia-induced atherosclerosis [1,2]. LDL-receptor-deficient and apoE-deficient mice have been in-tensively investigated in this regard. Chronic Ang II infu-sions in such mice accelerate atherosclerosis and promote aneurysm formation [3]. Angiotensin converting enzyme (ACE) inhibitors and angiotensin AT1 receptor blockers (ARB) reduce the atherosclerotic lesion size [3]. The results would suggest that reduced Ang II levels and decreased signalling through AT1 receptors are responsible for the salubrious effects of these drugs. However, some have ar-gued that perhaps increased signalling via AT2 receptor