Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
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The kallikrein-kinin system in diabetic nephropathyKinin B1 receptor enhances the oxidative stress in a rat model of insulin resistance: outcome in hypertension, allodynia and metabolic complicationsMitochondrial DNA polymerase editing mutation, PolgD257A, reduces the diabetic phenotype of Akita male mice by suppressing appetite.Plasma kininogen and kininogen fragments are biomarkers of progressive renal decline in type 1 diabetes.Mouse models of diabetic nephropathy.Plasma bradykinin and early diabetic nephropathy lesions in type 1 diabetes mellitusLack of both bradykinin B1 and B2 receptors enhances nephropathy, neuropathy, and bone mineral loss in Akita diabetic miceClassical Renin-Angiotensin system in kidney physiologyBradykinin decreases podocyte permeability through ADAM17-dependent epidermal growth factor receptor activation and zonula occludens-1 rearrangementLoss of bradykinin signaling does not accelerate the development of cardiac dysfunction in type 1 diabetic akita mice.Kinin B2 receptor does not exert renoprotective effects on mice with glycerol-induced rhabdomyolysis.Global renal gene expression profiling analysis in B2-kinin receptor null mice: impact of diabetesSenescence-associated phenotypes in Akita diabetic mice are enhanced by absence of bradykinin B2 receptors.From fibrosis to sclerosis: mechanisms of glomerulosclerosis in diabetic nephropathy.Loss of angiotensin-converting enzyme-2 leads to the late development of angiotensin II-dependent glomerulosclerosisEvaluation of Antidiabetic and Antihyperlipidemic Effects of Hydroalcoholic Extract of Leaves of Ocimum tenuiflorum (Lamiaceae) and Prediction of Biological Activity of its PhytoconstituentsBradykinin B1 and B2 receptors both have protective roles in renal ischemia/reperfusion injury.Loss of angiotensin-converting enzyme-2 (Ace2) accelerates diabetic kidney injuryDual RAS blockade normalizes angiotensin-converting enzyme-2 expression and prevents hypertension and tubular apoptosis in Akita angiotensinogen-transgenic mice.Characterization of dual agonists for kinin B1 and B2 receptors and their biased activation of B2 receptorsMany little things: one geneticist's view of complex diseases.Bradykinin B2 receptors--a target in diabetic nephropathy.Mechanisms of bradykinin-induced expression of connective tissue growth factor and nephrin in podocytes.Genetically altered animal models in the kallikrein-kinin system.Null mutations at the p66 and bradykinin 2 receptor loci induce divergent phenotypes in the diabetic kidney.Lack of A1 adenosine receptors augments diabetic hyperfiltration and glomerular injury.Kallikrein transduced mesenchymal stem cells protect against anti-GBM disease and lupus nephritis by ameliorating inflammation and oxidative stressThe kallikrein-kinin system in health and in diseases of the kidney.Inhibition of p66ShcA redox activity in cardiac muscle cells attenuates hyperglycemia-induced oxidative stress and apoptosis.Loss of angiotensin-converting enzyme-2 exacerbates diabetic cardiovascular complications and leads to systolic and vascular dysfunction: a critical role of the angiotensin II/AT1 receptor axisKallikrein genes are associated with lupus and glomerular basement membrane-specific antibody-induced nephritis in mice and humans.Plasma kallikrein mediates angiotensin II type 1 receptor-stimulated retinal vascular permeabilityNew insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy.Abnormalities in signaling pathways in diabetic nephropathy.Elevation of the antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline: a blood pressure-independent beneficial effect of angiotensin I-converting enzyme inhibitorsNew molecular insights in diabetic nephropathy.Diabetic nephropathy: lessons from the mouse.Human recombinant ACE2 reduces the progression of diabetic nephropathy.Ontogeny of bradykinin B1 receptors in the mouse kidney.The lupus-susceptibility gene kallikrein downmodulates antibody-mediated glomerulonephritis.
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Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
description
article científic
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article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
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scientific article published on 23 August 2004
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
@en
Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
@nl
type
label
Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
@en
Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
@nl
prefLabel
Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
@en
Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
@nl
P2093
P2860
P356
P1476
Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor.
@en
P2093
J Charles Jennette
Masao Kakoki
Nobuyuki Takahashi
P2860
P304
13302-13305
P356
10.1073/PNAS.0405449101
P407
P577
2004-08-23T00:00:00Z