ArticleThe American journal of pathology2011
Selective stimulation of VEGFR2 accelerates progressive renal disease.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Effects of low versus standard pressure pneumoperitoneum on renal syndecan-1 shedding and VEGF receptor-2 expression in living-donor nephrectomy: a randomized controlled study.BMC anesthesiology · 2020Trial
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Suramin Affects the Renal VEGF-A/VEGFR Axis in Short-Term Streptozotocin-Induced Diabetes.Pharmaceuticals (Basel, Switzerland) · 2023Article
- VEGFR2 insufficiency enhances phosphotoxicity and undermines Klotho's protection against peritubular capillary rarefaction and kidney fibrosis.American journal of physiology. Renal physiology · 2023Article
- Plasma proteomic characterization of the development of acute kidney injury in early sepsis patients.Scientific reports · 2022Article
- Glomerular endothelial cell-podocyte stresses and crosstalk in structurally normal kidney transplants.Kidney international · 2022Article
- The vascular protective effect of matrix Gla protein during kidney injury.Frontiers in molecular medicine · 2022Review
- Spatially Resolved Transcriptomes of Mammalian Kidneys Illustrate the Molecular Complexity and Interactions of Functional Nephron Segments.Frontiers in medicine · 2022Article
- Saccharin and Sucralose Protect the Glomerular Microvasculature In Vitro against VEGF-Induced Permeability.Nutrients · 2021Article
- Antiangiogenic therapy in diabetic nephropathy: A double‑edged sword (Review).Molecular medicine reports · 2021Review
- Capillary rarefaction from the kidney point of view.Clinical kidney journal · 2018Article
- Deletion of pro-angiogenic factor vasohibin-2 ameliorates glomerular alterations in a mouse diabetic nephropathy model.PloS one · 2018Article
- A LASSO Method to Identify Protein Signature Predicting Post-transplant Renal Graft Survival.Statistics in biosciences · 2017Article
- Antiangiogenic Therapy for Diabetic Nephropathy.BioMed research international · 2017Review
- Vascular endothelial growth factor: an attractive target in the treatment of hypoxic/ischemic brain injury.Neural regeneration research · 2016Review
- Impaired angiogenesis in the enalapril-treated neonatal rat kidney.Korean journal of pediatrics · 2016Article
- Blocking VEGF/Caveolin-1 signaling contributes to renal protection of fasudil in streptozotocin-induced diabetic rats.Acta pharmacologica Sinica · 2015Article
- Peritubular capillary rarefaction: a new therapeutic target in chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2014Review
- Uncoupling of VEGF with endothelial NO as a potential mechanism for abnormal angiogenesis in the diabetic nephropathy.Journal of diabetes research · 2013Review
- Restoring the renal microvasculature to treat chronic kidney disease.Nature reviews. Nephrology · 2012Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial growth factor A (VEGF-A) can play both beneficial and deleterious roles in renal diseases, where its specific function might be determined by nitric oxide bioavailability. The complexity of VEGF-A in renal disease could in part be accounted for by the distinct roles of its two receptors; VEGFR1 is involved in the inflammatory responses, whereas VEGFR2 predominantly mediates angiogenesis. Because nondiabetic chronic renal disease is associated with capillary loss, we hypothesized that selective stimulation of VEGFR2 could be beneficial in this setting. However, VEGFR2 activation may be deleterious in the presence of nitric oxide deficiency. We systematically overexpressed a mutant form of VEGF-A binding only VEGFR2 (Flk-sel) using an adeno-associated virus-1 vector in wild-type and eNOS knockout mice and then induced renal injury by uninephrectomy. Flk-sel treatment increased angiogenesis and lowered blood pressure in both mouse types. Flk-sel overexpression caused mesangial injury with increased proliferation associated with elevated expression of PDGF, PDGF-β receptor, and VEGFR2; this effect was greater in eNOS knockout than in wild-type mice. Flk-sel also induced tubulointerstitial injury, with some tubular epithelial cells expressing α-smooth muscle actin, indicating a phenotypic evolution toward myofibroblasts. In conclusion, prestimulation of VEGFR2 can potentiate subsequent renal injury in mice, an effect enhanced in the setting of nitric oxide deficiency.
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