Podocyte vascular endothelial growth factor (Vegf₁₆₄) overexpression causes severe nodular glomerulosclerosis in a mouse model of type 1 diabetes. - Wikidata - awgldk - TriplyDB

Podocyte vascular endothelial growth factor (Vegf₁₆₄) overexpression causes severe nodular glomerulosclerosis in a mouse model of type 1 diabetes.

Podocyte vascular endothelial growth factor (Vegf₁₆₄) overexpression causes severe nodular glomerulosclerosis in a mouse model of type 1 diabetes.

http://www.wikidata.org/entity/Q41822455

about

Insulin receptor substrate-2 is expressed in kidney epithelium and up-regulated in diabetic nephropathy Vascular Endothelial Growth Factor-A165b Is Protective and Restores Endothelial Glycocalyx in Diabetic Nephropathy Crosstalk in glomerular injury and repair Antiangiogenic treatment diminishes renal injury and dysfunction via regulation of local AKT in early experimental diabetes Acute podocyte vascular endothelial growth factor (VEGF-A) knockdown disrupts alphaVbeta3 integrin signaling in the glomerulus.Podocyte-specific VEGF-a gain of function induces nodular glomerulosclerosis in eNOS null mice.Increased urine semaphorin-3A is associated with renal damage in hypertensive patients with chronic kidney disease: a nested case-control study Semaphorin3a promotes advanced diabetic nephropathy Vascular endothelial growth factor receptor 2 direct interaction with nephrin links VEGF-A signals to actin in kidney podocytes Delayed Treatment with a Small Pigment Epithelium Derived Factor (PEDF) Peptide Prevents the Progression of Diabetic Renal Injury Twenty years after ACEIs and ARBs: emerging treatment strategies for diabetic nephropathy.VEGF165b overexpression restores normal glomerular water permeability in VEGF164-overexpressing adult mice.Vegfa protects the glomerular microvasculature in diabetes.Protective role of small pigment epithelium-derived factor (PEDF) peptide in diabetic renal injury.Podocytes: the Weakest Link in Diabetic Kidney Disease?Elevated expression levels of serum insulin-like growth factor-1, tumor necrosis factor-α and vascular endothelial growth factor 165 might exacerbate type 2 diabetic nephropathy.New insights into molecular mechanisms of diabetic kidney disease.Semaphorin3a signaling, podocyte shape, and glomerular disease.Semaphorins in kidney development and disease: modulators of ureteric bud branching, vascular morphogenesis, and podocyte-endothelial crosstalk.VEGF and podocytes in diabetic nephropathy.Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytes Therapeutic angiogenesis by vascular endothelial growth factor supplementation for treatment of renal disease.Vitamin D and its receptor regulate lipopolysaccharide-induced transforming growth factor-β, angiotensinogen expression and podocytes apoptosis through the nuclear factor-κB pathway Antiangiogenic Therapy for Diabetic Nephropathy.Excess podocyte semaphorin-3A leads to glomerular disease involving plexinA1-nephrin interaction.The vasculature in diabetic nephropathy: all tied up?Targeted glomerular angiopoietin-1 therapy for early diabetic kidney disease.Diabetic Microvascular Disease: An Endocrine Society Scientific Statement.VEGF levels in plasma in relation to metabolic control, inflammation, and microvascular complications in type-2 diabetes: A cohort study.Proteinuric Kidney Diseases: A Podocyte's Slit Diaphragm and Cytoskeleton Approach

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Podocyte vascular endothelial growth factor (Vegf₁₆₄) overexpression causes severe nodular glomerulosclerosis in a mouse model of type 1 diabetes.

http://www.wikidata.org/entity/Q41822455

description

2011 nî lūn-bûn

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2011年論文

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2011年論文

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2011年论文

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Podocyte vascular endothelial ...... ouse model of type 1 diabetes.

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Podocyte vascular endothelial ...... mouse model of type 1 diabetes

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A M Garcia

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A Marlier

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A Tufro

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C A Bertuccio

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D Veron

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H Velazquez

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J Jimenez

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K Reidy

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M Kashgarian

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P2860

Neuropilin is a semaphorin III receptor

VEGF inhibition and renal thrombotic microangiopathy

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Proteinuria and the expression of the podocyte slit diaphragm protein, nephrin, in diabetic nephropathy: effects of angiotensin converting enzyme inhibition

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

Lack of endothelial nitric-oxide synthase leads to progressive focal renal injury

Mouse models of diabetic nephropathy.

Induction of podocyte VEGF164 overexpression at different stages of development causes congenital nephrosis or steroid-resistant nephrotic syndrome

Major contribution of tubular secretion to creatinine clearance in mice.

Deficiency of endothelial nitric-oxide synthase confers susceptibility to diabetic nephropathy in nephropathy-resistant inbred mice.

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5

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Gilbert W Moeckel

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49833498

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21318407

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type-1 diabetes

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3397150

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