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The biology of the (pro)renin receptor

Item Type:Review
Title:The biology of the (pro)renin receptor
Creators Name:Nguyen, G. and Mueller, D.N.
Abstract:The (pro)renin receptor (PRR) binds renin and prorenin, its proenzyme inactive form. Receptor-bound prorenin becomes enzymatically active and binding then activates the MAP kinases ERK1/2 and p38 pathways, leading to upregulation of profibrotic and cyclooxygenase-2 genes independent of angiotensin II generation. These characteristics explain the interest in the potential role of PRR in organ damage in diseases associated with activation of the renin-angiotensin system (RAS), in particular hypertension and diabetes. Although identification of PRR has improved our understanding of the physiology of the tissue RAS, its role in pathology is far from clear. Transgenic animals overexpressing PRR ubiquitously or selectively in smooth-muscle cells develop high BP or glomerulosclerosis, and increased expression of PRR is reported in models of hypertension or kidney damage. However, definitive proof is still lacking for a role for PRR in disease, or by showing improvement of disease by tissue-specific ablation of PRR or by administration of a specific PRR antagonist. Furthermore, the early embryonic lethality seen in PRR-null mice suggests PRR has additional essential cellular functions we do not understand.
Keywords:Animal Disease Models, Extracellular Signal-Regulated MAP Kinases, Hypertension, Kidney Diseases, Cell Surface Receptors, Renin-Angiotensin System, Signal Transduction, Animals, Mice
Source:Journal of the American Society of Nephrology
Publisher:American Society of Nephrology
Page Range:18-23
Date:January 2010
Official Publication:https://doi.org/10.1681/ASN.2009030300
PubMed:View item in PubMed

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