Abstract
When the ‘handle region’ of the prorenin prosegment interacts with the (pro)renin receptor, the prorenin molecule partially changes the conformation to an enzymatically active state. On the other hand, the receptor triggers its own intracellular signalling pathways independent of the renin–angiotensin system (RAS). The ‘handle region’ peptide competitively binds to the receptor as a decoy peptide and inhibits both the non-proteolytic activation of prorenin and the RAS-independent intracellular signals. Therefore, prorenin receptor blockers including the decoy peptide may have superior benefits on end-organ damage in diabetes and hypertension compared with conventional RAS inhibitors.