ArticleAmerican journal of physiology. Renal physiology2010
FVB mouse genotype confers susceptibility to OVE26 diabetic albuminuria.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Optimizing diabetic kidney disease animal models: Insights from a meta-analytic approach.Animal models and experimental medicine · 2023Pooled it
- Recessive variants in the intergenic NOS1AP-C1orf226 locus cause monogenic kidney disease responsive to anti-proteinuric treatment.Nature communications · 2025Article
- Neutrophil heterogeneity and plasticity: unveiling the multifaceted roles in health and disease.MedComm · 2025Review
- LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- The single-cell landscape of kidney immune cells reveals transcriptional heterogeneity in early diabetic kidney disease.Kidney international · 2022Article
- Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.Advanced drug delivery reviews · 2021Review
- Diabetic fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Plasminogen Deficiency and Amiloride Mitigate Angiotensin II-Induced Hypertension in Type 1 Diabetic Mice Suggesting Effects Through the Epithelial Sodium Channel.Journal of the American Heart Association · 2020Article
- Therapeutic Effects of Fibroblast Growth Factor-21 on Diabetic Nephropathy and the Possible Mechanism in Type 1 Diabetes Mellitus Mice.Diabetes & metabolism journal · 2020Article
- Deletion of the Tensin2 SH2-PTB domain, but not the loss of its PTPase activity, induces podocyte injury in FVB/N mouse strain.Experimental animals · 2020Article
- Animal Models of Diabetes-Associated Renal Injury.Journal of diabetes research · 2020Review
- Tyro3 is a podocyte protective factor in glomerular disease.JCI insight · 2018Article
- Increased podocyte Sirtuin-1 function attenuates diabetic kidney injury.Kidney international · 2018Article
- Protein S Protects against Podocyte Injury in Diabetic Nephropathy.Journal of the American Society of Nephrology : JASN · 2018Article
- Modelling diabetic nephropathy in mice.Nature reviews. Nephrology · 2018Review
- 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
- Skin Exposure to Ultraviolet B Rapidly Activates Systemic Neuroendocrine and Immunosuppressive Responses.Photochemistry and photobiology · 2017Article
- Renoprotection From Diabetic Complications in OVE Transgenic Mice by Endothelial Cell Specific Overexpression of Metallothionein: A TEM Stereological Analysis.Anatomical record (Hoboken, N.J. : 2007) · 2017Article
- The Promise of Mesenchymal Stem Cell Therapy for Diabetic Kidney Disease.Current diabetes reports · 2016Review
- HIF-1 Mediates Renal Fibrosis in OVE26 Type 1 Diabetic Mice.Diabetes · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
OVE26 (OVE) diabetic mice on the inbred strain FVB are a valuable model of diabetic nephropathy that excretes the highest amount of urine albumin of all diabetic mouse models. Crossing of OVE mice to C57BL6 or DBA2 mice reduced albuminuria 17-fold in F1 diabetic offspring without reducing diabetes. When comparing renal histology of OVE mice on the FVB background to F1 C57BL6 crosses, we found that the F1 kidneys had significantly smaller glomeruli, much less albumin accumulation in tubules, reduced mesangial matrix expansion, and less interstitial fibrosis. A genome scan of 108 OVE-positive N2 offspring for albuminuria revealed one significant peak on chromosome 11 and nearly significant peaks on chromosomes 9, 13, and 19. Homozygosity for the FVB genotype for peaks on chromosomes 11, 13, or 19 increased albuminuria. Homozygosity for the chromosome 9 peak reduced albuminuria. Combined homozyogosity for the peaks on chromosomes 11, 13, and 19 increased albuminuria over 12-fold and accounted for >70% of the difference between OVE mice on the FVB vs. the F1 background. These loci contain sequences important to susceptibility to diabetic albuminuria.
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