Inducible overexpression of sFlt-1 in podocytes ameliorates glomerulopathy in diabetic mice - Wikidata - awgldk - TriplyDB

Inducible overexpression of sFlt-1 in podocytes ameliorates glomerulopathy in diabetic mice

Inducible overexpression of sFlt-1 in podocytes ameliorates glomerulopathy in diabetic mice

http://www.wikidata.org/entity/Q36906413

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Renal endothelial dysfunction in diabetic nephropathy Crosstalk in glomerular injury and repair Deletion of von Hippel-Lindau in glomerular podocytes results in glomerular basement membrane thickening, ectopic subepithelial deposition of collagen {alpha}1{alpha}2{alpha}1(IV), expression of neuroglobin, and proteinuria.Podocyte-specific overexpression of GLUT1 surprisingly reduces mesangial matrix expansion in diabetic nephropathy in mice Modulation of notch-1 signaling alleviates vascular endothelial growth factor-mediated diabetic nephropathy.Angiogenesis and chronic kidney disease.Mechanism of kidney injury caused by bevacizumab in rats Induction of podocyte-derived VEGF ameliorates podocyte injury and subsequent abnormal glomerular development caused by puromycin aminonucleoside Glomerular endothelial cell injury and cross talk in diabetic kidney disease Relevance of VEGF and nephrin expression in glomerular diseases.Vascular endothelial growth factor receptor 2 direct interaction with nephrin links VEGF-A signals to actin in kidney podocytes Glomerular VEGF resistance induced by PKCδ/SHP-1 activation and contribution to diabetic nephropathy.Twenty years after ACEIs and ARBs: emerging treatment strategies for diabetic nephropathy.Vegfa protects the glomerular microvasculature in diabetes.Albuminuria is associated with too few glomeruli and too much testosterone Role of the eNOS-NO system in regulating the antiproteinuric effects of VEGF receptor 2 inhibition in diabetes.Abnormal angiogenesis in diabetic nephropathy.Endothelial-podocyte crosstalk: the missing link between endothelial dysfunction and albuminuria in diabetes.Vasohibin-1, a negative feedback regulator of angiogenesis, ameliorates renal alterations in a mouse model of diabetic nephropathy.Diabetes-Induced Reactive Oxygen Species: Mechanism of Their Generation and Role in Renal Injury Cellular and molecular mechanisms of diabetic glomerulopathy.VEGF and podocytes in diabetic nephropathy.The renal endothelium in diabetic nephropathy.Pathophysiology of the diabetic kidney.Uncoupling of VEGF with endothelial NO as a potential mechanism for abnormal angiogenesis in the diabetic nephropathy.Signal transduction in podocytes--spotlight on receptor tyrosine kinases.Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytes From Glomerular Endothelium to Podocyte Pathobiology in Preeclampsia: a Paradigm Shift.PACSIN2 accelerates nephrin trafficking and is up-regulated in diabetic kidney disease.Gremlin regulates renal inflammation via the vascular endothelial growth factor receptor 2 pathway.Endothelial factors and diabetic nephropathy.The VEGF-A inhibitor sFLT-1 improves renal function by reducing endothelial activation and inflammation in a mouse model of type 1 diabetes.Antiangiogenic Therapy for Diabetic Nephropathy.Glomerular structure and function require paracrine, not autocrine, VEGF-VEGFR-2 signaling.Impaired Albumin Uptake and Processing Promote Albuminuria in OVE26 Diabetic Mice.Podocyte vascular endothelial growth factor (Vegf₁₆₄) overexpression causes severe nodular glomerulosclerosis in a mouse model of type 1 diabetes.The vasculature in diabetic nephropathy: all tied up?Targeted glomerular angiopoietin-1 therapy for early diabetic kidney disease.Soluble Flt-1 gene therapy ameliorates albuminuria but accelerates tubulointerstitial injury in diabetic mice.Long-term blockade of vascular endothelial growth factor receptor-2 aggravates the diabetic renal dysfunction associated with inactivation of the Akt/eNOS-NO axis.

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Inducible overexpression of sFlt-1 in podocytes ameliorates glomerulopathy in diabetic mice

http://www.wikidata.org/entity/Q36906413

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2008年论文

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Alessandra Dei Cas

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Anthea Hayward

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Ching-Hsin Ku

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Giancarlo Viberti

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Kathryn E White

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Luigi Gnudi

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Rudy Bilous

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Sally Marshall

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Zoe Webster

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P2860

Inhibition of vascular endothelial cell growth factor activity by an endogenously encoded soluble receptor

Different signal transduction properties of KDR and Flt1, two receptors for vascular endothelial growth factor

VEGF inhibition and renal thrombotic microangiopathy

The biology of VEGF and its receptors

Signal transduction via vascular endothelial growth factor (VEGF) receptors and their roles in atherogenesis

Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia

Nephrin in experimental glomerular disease.

Molecular basis of glomerular permselectivity.

Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases.

Long-term prevention of renal insufficiency, excess matrix gene expression, and glomerular mesangial matrix expansion by treatment with monoclonal antitransforming growth factor-beta antibody in db/db diabetic mice.

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18647955

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