Senescence-associated phenotypes in Akita diabetic mice are enhanced by absence of bradykinin B2 receptors.
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Animal models of diabetic macrovascular complications: key players in the development of new therapeutic approachesThe kallikrein-kinin system in diabetic nephropathyThe kallikrein-kinin system and oxidative stressKinin 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.Calorie restriction enhances cell adaptation to hypoxia through Sirt1-dependent mitochondrial autophagy in mouse aged kidney.Mouse models of diabetic nephropathy.Lack of both bradykinin B1 and B2 receptors enhances nephropathy, neuropathy, and bone mineral loss in Akita diabetic miceClassical Renin-Angiotensin system in kidney physiologyLoss of bradykinin signaling does not accelerate the development of cardiac dysfunction in type 1 diabetic akita mice.Prevention of diabetic nephropathy in Ins2(+/)⁻(AkitaJ) mice by the mitochondria-targeted therapy MitoQ.From fibrosis to sclerosis: mechanisms of glomerulosclerosis in diabetic nephropathy.Bradykinin inhibits oxidative stress-induced cardiomyocytes senescence via regulating redox state.SOD1, but not SOD3, deficiency accelerates diabetic renal injury in C57BL/6-Ins2(Akita) diabetic miceThe identification of gene expression profiles associated with progression of human diabetic neuropathyBradykinin B1 and B2 receptors both have protective roles in renal ischemia/reperfusion injury.P2X7R-Panx1 Complex Impairs Bone Mechanosignaling under High Glucose Levels Associated with Type-1 DiabetesBradykinin inhibits oxidative stress-induced senescence of endothelial progenitor cells through the B2R/AKT/RB and B2R/EGFR/RB signal pathways.Null mutations at the p66 and bradykinin 2 receptor loci induce divergent phenotypes in the diabetic kidney.The role of the renal kallikrein-kinin system in diabetic nephropathy.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.New insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy.Genetic deficiency in tissue kallikrein activity in mouse and man: effect on arteries, heart and kidney.The RHOX homeodomain proteins regulate the expression of insulin and other metabolic regulators in the testis.Loss of caveolin-1 and adiponectin induces severe inflammatory lung injury following LPS challenge through excessive oxidative/nitrative stress.Abnormalities in signaling pathways in diabetic nephropathy.Bradykinin type-2 receptor expression correlates with age and is subjected to transcriptional regulation.New molecular insights in diabetic nephropathy.Diabetic nephropathy: lessons from the mouse.Helix 8 plays a crucial role in bradykinin B(2) receptor trafficking and signaling.Angiotensin-converting enzyme inhibitors reduce oxidative stress intensity in hyperglicemic conditions in rats independently from bradykinin receptor inhibitors.Ontogeny of bradykinin B1 receptors in the mouse kidney.Resveratrol improves oxidative stress and protects against diabetic nephropathy through normalization of Mn-SOD dysfunction in AMPK/SIRT1-independent pathway.Binding characteristics of [3H]-JSM10292: a new cell membrane-permeant non-peptide bradykinin B2 receptor antagonist.Beyond glucose: metabolic shifts in responses to the effects of the oral glucose tolerance test and the high-fructose diet in rats.KRAS, YAP, and obesity in pancreatic cancer: A signaling network with multiple loops.
P2860
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P2860
Senescence-associated phenotypes in Akita diabetic mice are enhanced by absence of bradykinin B2 receptors.
description
2006 nî lūn-bûn
@nan
2006 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@ast
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@en
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@nl
type
label
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@ast
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@en
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@nl
prefLabel
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@ast
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@en
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@nl
P2093
P2860
P356
P1476
Senescence-associated phenotyp ...... ce of bradykinin B2 receptors.
@en
P2093
C Robert Bagnell
Catherine M Kizer
Cora-Jean S Edgell
Hyung-Suk Kim
J Charles Jennette
Masao Kakoki
Nobuyo Maeda
Nobuyuki Takahashi
Xianwen Yi
P2860
P304
P356
10.1172/JCI26958
P407
P577
2006-04-06T00:00:00Z