ArticleJournal of the American Society of Nephrology : JASN2014
Podocyte-specific VEGF-a gain of function induces nodular glomerulosclerosis in eNOS null mice.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Effect of empagliflozin on urinary albumin excretion and hypoxic biomarkers in early diabetic kidney disease: A randomised double-blind, placebo-controlled trial.Diabetes, obesity & metabolism · 2026Trial
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Systemic Effects of Intravitreal Anti-VEGF Therapy: A Review of Safety across Organ Systems.Ophthalmology and therapy · 2025Review
- Chronic Kidney Disease of Unknown Etiology: A Global Health Threat in Rural Agricultural Communities-Prevalence, Suspected Causes, Mechanisms, and Prevention Strategies.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Review
- Pro- and anti-fibrotic effects of vascular endothelial growth factor in chronic kidney diseases.Renal failure · 2022Review
- Glomerular cell cross talk in diabetic kidney diseases.Journal of diabetes · 2022Review
- Comprehensive analyses of the microRNA-messenger RNA-transcription factor regulatory network in mouse and human renal fibrosis.Frontiers in genetics · 2022Article
- SGLT2 inhibitors suppress epithelial-mesenchymal transition in podocytes under diabetic conditionsFrontiers in pharmacology · 2022Article
- Role of Endothelial Glucocorticoid Receptor in the Pathogenesis of Kidney Diseases.International journal of molecular sciences · 2021Review
- Rho-GTPase Activating Protein myosin MYO9A identified as a novel candidate gene for monogenic focal segmental glomerulosclerosis.Kidney international · 2021Article
- S-Nitrosylation in Tumor Microenvironment.International journal of molecular sciences · 2021Review
- S-Nitrosylation of RhoGAP Myosin9A Is Altered in Advanced Diabetic Kidney Disease.Frontiers in medicine · 2021Article
- PodocyteFrontiers in pharmacology · 2021Article
- Targeting angiogenesis and lymphangiogenesis in kidney disease.Nature reviews. Nephrology · 2020Review
- Agonistic anti-CD148 monoclonal antibody attenuates diabetic nephropathy in mice.American journal of physiology. Renal physiology · 2020Article
- Role of VEGF-A and LRG1 in Abnormal Angiogenesis Associated With Diabetic Nephropathy.Frontiers in physiology · 2020Review
- Glomerular Endothelial Cells as Instigators of Glomerular Sclerotic Diseases.Frontiers in pharmacology · 2020Review
- S-Nitrosylation: An Emerging Paradigm of Redox Signaling.Antioxidants (Basel, Switzerland) · 2019Review
- Friends Turned Foes: Angiogenic Growth Factors beyond Angiogenesis.Biomolecules · 2017Review
- Antiangiogenic Therapy for Diabetic Nephropathy.BioMed research international · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
VEGF-A and nitric oxide are essential for glomerular filtration barrier homeostasis and are dysregulated in diabetic nephropathy. Here, we examined the effect of excess podocyte VEGF-A on the renal phenotype of endothelial nitric oxide synthase (eNOS) knockout mice. Podocyte-specific VEGF(164) gain of function in eNOS(-/-) mice resulted in nodular glomerulosclerosis, mesangiolysis, microaneurysms, and arteriolar hyalinosis associated with massive proteinuria and renal failure in the absence of diabetic milieu or hypertension. In contrast, podocyte-specific VEGF(164) gain of function in wild-type mice resulted in less pronounced albuminuria and increased creatinine clearance. Transmission electron microscopy revealed glomerular basement membrane thickening and podocyte effacement in eNOS(-/-) mice with podocyte-specific VEGF(164) gain of function. Furthermore, glomerular nodules overexpressed collagen IV and laminin extensively. Biotin-switch and proximity ligation assays demonstrated that podocyte-specific VEGF(164) gain of function decreased glomerular S-nitrosylation of laminin in eNOS(-/-) mice. In addition, treatment with VEGF-A decreased S-nitrosylated laminin in cultured podocytes. Collectively, these data indicate that excess glomerular VEGF-A and eNOS deficiency is necessary and sufficient to induce Kimmelstiel-Wilson-like nodular glomerulosclerosis in mice through a process that involves deposition of laminin and collagen IV and de-nitrosylation of laminin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.