Abstract
The renin–angiotensin system (RAS) plays pivotal roles in homeostasis, but its abnormal activation has been proposed as a risk factor for several disorders including diabetes. Using animal models, we previously clarified the molecular mechanisms in which tissue RAS stimulates retinal angiogenesis and the critical roles of (pro)renin receptor [(P)RR] in retinal RAS activation and its concurrent intracellular signal transduction, i.e., the receptor-associated prorenin system (RAPS). Most recently, we have revealed that (P)RR is associated with vascular endothelial growth factor (VEGF)-driven angiogenic activity in human proliferative diabetic retinopathy (DR), and also showed a close relationship between vitreous renin activity and VEGF-induced pathogenesis of DR. These findings suggest that both vitreous RAS and retinal RAPS are tightly linked to the molecular pathogenesis of DR.
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