ArticleDiabetologia2017
The VEGF-A inhibitor sFLT-1 improves renal function by reducing endothelial activation and inflammation in a mouse model of type 1 diabetes.
Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- 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
- The role of the vascular niche in regulating kidney tubulointerstitial fibrosis.Kidney international · 2026Review
- Identification of transcription factors that regulate placental sFLT1 expression.Molecular human reproduction · 2025Article
- Article
- Exploring the Molecular Modalities in the Pathogenesis of Diabetic Kidney Disease with a Focus on the Potential Therapeutic Implications.Biomedicines · 2024Review
- The construction of elastin-like polypeptides and their applications in drug delivery system and tissue repair.Journal of nanobiotechnology · 2023Review
- MIF Increases sFLT1 Expression in Early Uncomplicated Pregnancy and Preeclampsia.International journal of molecular sciences · 2023Article
- Relationship between serum fibroblast growth factor 19 and vascular endothelial growth factor and soluble klotho protein in type 1 diabetic children.BMC pediatrics · 2023Article
- Bioinformatics Analysis of Next Generation Sequencing Data Identifies Molecular Biomarkers Associated With Type 2 Diabetes Mellitus.Clinical medicine insights. Endocrinology and diabetes · 2023Article
- Pro- and anti-fibrotic effects of vascular endothelial growth factor in chronic kidney diseases.Renal failure · 2022Review
- The VEGF Inhibitor Soluble Fms-like Tyrosine Kinase 1 Does Not Promote AKI-to-CKD Transition.International journal of molecular sciences · 2022Article
- microRNA-15b-5p shuttled by mesenchymal stem cell-derived extracellular vesicles protects podocytes from diabetic nephropathy via downregulation of VEGF/PDK4 axis.Journal of bioenergetics and biomembranes · 2022Article
- Stem cell-derived and circulating exosomal microRNAs as new potential tools for diabetic nephropathy management.Stem cell research & therapy · 2022Review
- Research progress on exosomes/microRNAs in the treatment of diabetic retinopathy.Frontiers in endocrinology · 2022Review
- Exosomal microRNA-16-5p from human urine-derived stem cells ameliorates diabetic nephropathy through protection of podocyte.Journal of cellular and molecular medicine · 2021Article
- Study of the Active Components and Molecular Mechanism ofFrontiers in molecular biosciences · 2021Article
- Exosomes: Biomarkers and Therapeutic Targets of Diabetic Vascular Complications.Frontiers in endocrinology · 2021Review
- Glomerular clusterin expression is increased in diabetic nephropathy and protects against oxidative stress-induced apoptosis in podocytes.Scientific reports · 2020Article
- Changes of expression levels of serum cystatin C and soluble vascular endothelial growth factor receptor 1 in the treatment of patients with glomerulus nephritis.Experimental and therapeutic medicine · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisAnimal models of diabetic nephropathy show increased levels of glomerular vascular endothelial growth factor (VEGF)-A, and several studies have shown that inhibiting VEGF-A in animal models of diabetes can prevent albuminuria and glomerular hypertrophy. However, in those studies, treatment was initiated before the onset of kidney damage. Therefore, the aim of this study was to investigate whether transfecting mice with the VEGF-A inhibitor sFlt-1 (encoding soluble fms-related tyrosine kinase 1) can reverse pre-existing kidney damage in a mouse model of type 1 diabetes. In addition, we investigated whether transfection with sFlt-1 can reduce endothelial activation and inflammation in these mice.
methodsSubgroups of untreated 8-week-old female C57BL/6J control (n = 5) and diabetic mice (n = 7) were euthanised 5 weeks after the start of the experiment in order to determine the degree of kidney damage prior to treatment with sFLT-1. Diabetes was induced with three i.p. injections of streptozotocin (75 mg/kg) administered at 2 day intervals. Diabetic nephropathy was then investigated in diabetic mice transfected with sFlt-1 (n = 6); non-diabetic, non-transfected control mice (n = 5); non-diabetic control mice transfected with sFlt-1(n = 10); and non-transfected diabetic mice (n = 6). These mice were euthanised at the end of week 15. Transfection with sFlt-1 was performed in week 6.
resultsWe found that transfection with sFlt-1 significantly reduced kidney damage by normalising albuminuria, glomerular hypertrophy and mesangial matrix content (i.e. glomerular collagen type IV protein levels) (p < 0.001). We also found that transfection with sFlt-1 reduced endothelial activation (p < 0.001), glomerular macrophage infiltration (p < 0.001) and glomerular TNF-α protein levels (p < 0.001). Finally, sFLT-1 decreased VEGF-A-induced endothelial activation in vitro (p < 0.001). CONCLUSIONS/
interpretationThese results suggest that sFLT-1 might be beneficial in treating diabetic nephropathy by inhibiting VEGF-A, thereby reducing endothelial activation and glomerular inflammation, and ultimately reversing kidney damage.
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