ArticleDiabetes2008
Inducible overexpression of sFlt-1 in podocytes ameliorates glomerulopathy in diabetic mice.
Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 101 citations in OpenAlex.
- Vascular Endothelial Growth Factor and Placental Growth Factor in Conjunction with Vascular Endothelial Growth Factor Receptor-1 May Exert Dual Effects Within the Kidney and Brain in Patients with Type 2 Diabetes Mellitus and Normoalbuminuric Diabetic Kidney Disease.International journal of molecular sciences · 2026Article
- Crosstalk mechanisms between glomerular endothelial cells and podocytes in renal diseases and kidney transplantation.Kidney research and clinical practice · 2024Article
- Inducing Angiogenesis in the Nucleus Pulposus.Cells · 2023Article
- Role of insulin signaling and its associated signaling in glomerulus for diabetic kidney disease.Histology and histopathology · 2023Review
- Antiangiogenic therapy in diabetic nephropathy: A double‑edged sword (Review).Molecular medicine reports · 2021Review
- Nephrotoxicity of Anti-Angiogenic Therapies.Diagnostics (Basel, Switzerland) · 2021Review
- Placental and maternal sFlt1/PlGF expression in gestational diabetes mellitus.Scientific reports · 2021Article
- Overexpression of Circulating Soluble Nogo-B Improves Diabetic Kidney Disease by Protecting the Vasculature.Diabetes · 2019Article
- Review
- Assessment of the SFlt-1 and sFlt-1/25(OH)D Ratio as a Diagnostic Tool in Gestational Hypertension (GH), Preeclampsia (PE), and Gestational Diabetes Mellitus (GDM).Disease markers · 2019Article
- Endogenous Antiangiogenic Factors in Chronic Kidney Disease: Potential Biomarkers of Progression.International journal of molecular sciences · 2018Review
- PACSIN2 accelerates nephrin trafficking and is up-regulated in diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- The VEGF-A inhibitor sFLT-1 improves renal function by reducing endothelial activation and inflammation in a mouse model of type 1 diabetes.Diabetologia · 2017Article
- Diabetes-Induced Reactive Oxygen Species: Mechanism of Their Generation and Role in Renal Injury.Journal of diabetes research · 2017Review
- Antiangiogenic Therapy for Diabetic Nephropathy.BioMed research international · 2017Review
- Impaired Albumin Uptake and Processing Promote Albuminuria in OVE26 Diabetic Mice.Journal of diabetes research · 2016Article
- Vascular Growth Factors and Glomerular Disease.Annual review of physiology · 2016Review
- Twenty years after ACEIs and ARBs: emerging treatment strategies for diabetic nephropathy.American journal of physiology. Renal physiology · 2015Review
- From Glomerular Endothelium to Podocyte Pathobiology in Preeclampsia: a Paradigm Shift.Current hypertension reports · 2015Review
- Crosstalk in glomerular injury and repair.Current opinion in nephrology and hypertension · 2015Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
objectivePodocyte-specific, doxycycline (DOX)-inducible overexpression of soluble vascular endothelial growth factor (VEGF) receptor-1 (sFlt-1) in adult mice was used to investigate the role of the VEGF-A/VEGF receptor (VEGFR) system in diabetic glomerulopathy. RESEARCH DESIGN AND
methodsWe studied nondiabetic and diabetic transgenic mice and wild-type controls treated with vehicle (VEH) or DOX for 10 weeks. Glycemia was measured by a glucose-oxidase method and blood pressure by a noninvasive technique. sFlt-1, VEGF-A, VEGFR2, and nephrin protein expression in renal cortex were determined by Western immunoblotting; urine sFlt-1, urine free VEGF-A, and albuminuria by enzyme-linked immunosorbent assay; glomerular ultrastructure by electron microscopy; and VEGFR1 and VEGFR2 cellular localization with Immunogold techniques.
resultsNondiabetic DOX-treated transgenic mice showed a twofold increase in cortex sFlt-1 expression and a fourfold increase in sFlt-1 urine excretion (P < 0.001). Urine free VEGF-A was decreased by 50%, and cortex VEGF-A expression was upregulated by 30% (P < 0.04). VEGFR2 expression was unchanged, whereas its activation was reduced in DOX-treated transgenic mice (P < 0.02). Albuminuria and glomerular morphology were similar among groups. DOX-treated transgenic diabetic mice showed a 60% increase in 24-h urine sFlt-1 excretion and an approximately 70% decrease in urine free VEGF-A compared with VEH-treated diabetic mice (P < 0.04) and had lower urine albumin excretion at 10 weeks than VEH-treated diabetic (d) mice: d-VEH vs. d-DOX, geometric mean (95% CI), 117.5 (69-199) vs. 43 (26.8-69) mug/24 h (P = 0.003). Diabetes-induced mesangial expansion, glomerular basement membrane thickening, podocyte foot-process fusion, and transforming growth factor-beta1 expression were ameliorated in DOX-treated diabetic animals (P < 0.05). Diabetes-induced VEGF-A and nephrin expression were not affected in DOX-treated mice.
conclusionsPodocyte-specific sFlt-1 overexpression ameliorates diabetic glomerular injury, implicating VEGF-A in the pathogenesis of this complication.
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