pro renin/proteinuria

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Physiology and pharmacology of the (pro)renin receptor.

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The (pro)renin receptor [(P)RR] is a single trans-membrane domain receptor that mediates renin and prorenin specific effects. The receptor acts as co-factor for renin and prorenin by increasing their enzymatic activity on the cell-surface and it activates the mitogen activated protein kinases ERK1/2

A (pro)renin receptor decoy peptide PRO20 protects against adriamycin-induced nephropathy by targeting intrarenal renin-angiotensin system

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Adriamycin (ADR) administration in susceptible rodents such as the BALB/c mouse strain produces injury to the glomerulus mimicking human chronic kidney disease (CKD) due to primary focal segmental glomerulosclerosis. The goal of the present study was to use this model to investigate antiproteinuric

Involvement of (pro)renin receptor in the glomerular filtration barrier.

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(Pro)renin receptor-bound prorenin not only causes the generation of angiotensin II via the nonproteolytic activation of prorenin, it also activates the receptor's own intracellular signaling pathways independent of the generated angiotensin II. Within the kidneys, the (pro)renin receptor is not

COX-2-Independent Activation of Renal (Pro)Renin Receptor Contributes to DOCA-Salt Hypertension in Rats

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It's been shown that COX-2-dependent activation of renal (pro)renin receptor (PRR) contributes to angiotensin II (AngII)-induced hypertension. However, less is known about the involvement of this mechanism in AngII-independent hypertension. The goal of the present study was to test whether or not

The Effect of Combined Treatment with the (Pro)Renin Receptor Blocker HRP and Quinapril in Type 1 Diabetic Rats.

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OBJECTIVE Diabetic nephropathy remains a major clinical problem. The effects of prorenin might be adverse, but the literature data are controversial. We compared the renal effects of the (pro)renin receptor ((P)RR) blockade and angiotensin converting enzyme (ACE) inhibition on the progression of

Renoprotective effects of mineralocorticoid receptor blockade in heminephrectomized (pro)renin receptor transgenic rats.

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1. Nephropathy and elevated plasma aldosterone concentrations (PAC) have been observed in (pro)renin receptor transgenic (TG) rats. In the present study, we hypothesized that PAC and/or mineralocorticoid receptor contribute to the nephropathy of TG rats. To test this hypothesis, the effects of a

(Pro)renin receptor and autophagy in podocytes.

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Within the kidneys, podocytes are highly specialized postmitotic cells. Podocytes, together with endothelial cells and the glomerular basement membrane (GBM), maintain the filtration barrier and the normal structure of the glomerular capillary, are involved in the remodeling of the GBM and the

Renal medullary (pro)renin receptor contributes to angiotensin II-induced hypertension in rats via activation of the local renin-angiotensin system.

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BACKGROUND (Pro)renin receptor (PRR) is a new component of the renin-angiotensin system and regulates renin activity in vitro. Within the kidney, PRR is highly expressed in the renal medulla where its expression is induced by angiotensin II infusion. The objective of the present study was to test a

Slowly progressive, angiotensin II-independent glomerulosclerosis in human (pro)renin receptor-transgenic rats.

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For defining the pathogenic effects of the (pro)renin receptor-transgenic rat, strains that overexpressed the human receptor were generated. Although transgenic rats were normotensive and euglycemic and had a renal angiotensin II (AngII) level that was comparable to that of wild-type rats,

Deterioration of kidney function by the (pro)renin receptor blocker handle region peptide in aliskiren-treated diabetic transgenic (mRen2)27 rats.

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Dual renin-angiotensin system (RAS) blockade in diabetic nephropathy is no longer feasible because of the profit/side effect imbalance. (Pro)renin receptor [(P)RR] blockade with handle region peptide (HRP) has been reported to exert beneficial effects in various diabetic models in a RAS-independent

(Pro)renin receptor promotes crescent formation via the ERK1/2 and Wnt/β-catenin pathways in glomerulonephritis

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(Pro)renin receptor ((P)RR) has multiple functions, but its regulation and role in the pathogenesis in glomerulonephritis (GN) are poorly defined. The aims of this study were to determine the effects of direct renin inhibition (DRI) and demonstrate the role of (P)RR on the progression of crescentic

Functional characterization of (pro)renin receptor in association with V-ATPase.

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The (pro)renin receptor ((P)RR) is a unique molecule that binds prorenin and renin in tissues, not only leading to their activation, but also inducing intracellular signaling. As a key player in the local renin-angiotensin system, (P)RR activation plays an important role in the development of

Podocyte COX-2 exacerbates diabetic nephropathy by increasing podocyte (pro)renin receptor expression.

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Diabetic nephropathy (DN) increases podocyte cyclooxygenase-2 (COX-2) expression, and COX-2 inhibition reduces proteinuria and glomerular injury in animal models of diabetes. To investigate the role of podocyte COX-2 in development of diabetic nephropathy, we employed a streptozotocin model of

Elevation of (Pro)Renin and (Pro)Renin Receptor in Preeclampsia.

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OBJECTIVE Preeclampsia (preE), a syndrome of hypertension, proteinuria, and edema, has many elusive triggers. The renin-angiotensin system has been implicated in preE pathogenesis. In this study, we test the hypothesis that (pro)renin levels are increased in preE patients and that levels of

Nebivolol attenuates redox-sensitive glomerular and tubular mediated proteinuria in obese rats.

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Obesity and insulin resistance-related proteinuria is associated with oxidative stress and impaired tissue bioavailable nitric oxide. Recent data suggest that nicotinamide adenine dinucleotide phosphate oxidase-mediated oxidative injury to the proximal tubule, like that seen in the glomerulus,

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