ArticlePloS one2014
Exacerbation of diabetic renal alterations in mice lacking vasohibin-1.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Review
- Article
- Antiangiogenic therapy in diabetic nephropathy: A double‑edged sword (Review).Molecular medicine reports · 2021Review
- Vasohibin-1 rescues erectile function through up-regulation of angiogenic factors in the diabetic mice.Scientific reports · 2021Article
- Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury.International journal of molecular sciences · 2020Article
- Targeting angiogenesis and lymphangiogenesis in kidney disease.Nature reviews. Nephrology · 2020Review
- Loss of Roundabout Guidance Receptor 2 (Robo2) in Podocytes Protects Adult Mice from Glomerular Injury by Maintaining Podocyte Foot Process Structure.The American journal of pathology · 2020Article
- VASH-1 Regulates Oxidative Stress and Fibrosis in Diabetic Kidney Disease via SIRT1/HIF1α and TGFβ1/Smad3 Signaling Pathways.Frontiers in molecular biosciences · 2020Article
- Role of VEGF-A and LRG1 in Abnormal Angiogenesis Associated With Diabetic Nephropathy.Frontiers in physiology · 2020Review
- Endogenous Antiangiogenic Factors in Chronic Kidney Disease: Potential Biomarkers of Progression.International journal of molecular sciences · 2018Review
- Double-Face of Vasohibin-1 for the Maintenance of Vascular Homeostasis and Healthy Longevity.Journal of atherosclerosis and thrombosis · 2018Review
- Deletion of pro-angiogenic factor vasohibin-2 ameliorates glomerular alterations in a mouse diabetic nephropathy model.PloS one · 2018Article
- Antiangiogenic Therapy for Diabetic Nephropathy.BioMed research international · 2017Review
- Knockout of Vasohibin-1 Gene in Mice Results in Healthy Longevity with Reduced Expression of Insulin Receptor, Insulin Receptor Substrate 1, and Insulin Receptor Substrate 2 in Their White Adipose Tissue.Journal of aging research · 2017Article
- Article
- Article
- Crosstalk in glomerular injury and repair.Current opinion in nephrology and hypertension · 2015Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vasohibin-1 (VASH1) is a unique endogenous inhibitor of angiogenesis that is induced in endothelial cells by pro-angiogenic factors. We previously reported renoprotective effect of adenoviral delivery of VASH1 in diabetic nephropathy model, and herein investigated the potential protective role of endogenous VASH1 by using VASH1-deficient mice. Streptozotocin-induced type 1 diabetic VASH1 heterozygous knockout mice (VASH1(+/-)) or wild-type diabetic mice were sacrificed 16 weeks after inducing diabetes. In the diabetic VASH1(+/-) mice, albuminuria were significantly exacerbated compared with the diabetic wild-type littermates, in association with the dysregulated distribution of glomerular slit diaphragm related proteins, nephrin and ZO-1, glomerular basement membrane thickening and reduction of slit diaphragm density. Glomerular monocyte/macrophage infiltration and glomerular nuclear translocation of phosphorylated NF-κB p65 were significantly exacerbated in the diabetic VASH1(+/-) mice compared with the diabetic wild-type littermates, accompanied by the augmentation of VEGF-A, M1 macrophage-derived MCP-1 and phosphorylation of IκBα, and the decrease of angiopoietin-1/2 ratio and M2 macrophage-derived Arginase-1. The glomerular CD31(+) endothelial area was also increased in the diabetic VASH1(+/-) mice compared with the diabetic-wild type littermates. Furthermore, the renal and glomerular hypertrophy, glomerular accumulation of mesangial matrix and type IV collagen and activation of renal TGF-β1/Smad3 signaling, a key mediator of renal fibrosis, were exacerbated in the diabetic VASH1(+/-) mice compared with the diabetic wild-type littermates. In conditionally immortalized mouse podocytes cultured under high glucose condition, transfection of VASH1 small interfering RNA (siRNA) resulted in the reduction of nephrin, angiopoietin-1 and ZO-1, and the augmentation of VEGF-A compared with control siRNA. These results suggest that endogenous VASH1 may regulate the development of diabetic renal alterations, partly via direct effects on podocytes, and thus, a strategy to recover VASH1 might potentially lead to the development of a novel therapeutic approach for diabetic nephropathy.
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