ArticleEndocrinology2014
Blocking ligand occupancy of the αVβ3 integrin inhibits the development of nephropathy in diabetic pigs.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Eleven genomic loci affect plasma levels of chronic inflammation marker soluble urokinase-type plasminogen activator receptor.Communications biology · 2021Pooled it
- Renal Single-Cell RNA Sequencing and Digital Cytometry in Dogs with X-Linked Hereditary Nephropathy.Animals : an open access journal from MDPI · 2025Article
- Umbilical Cord Mesenchymal Stem Cells Attenuate Podocyte Injury in Diabetic Nephropathy Rats by Inhibiting Angpltl4/IntegrinJournal of diabetes research · 2025Article
- The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024Review
- Article
- Cell Adhesion Molecules in Fibrotic Diseases.Biomedicines · 2023Review
- Functional and morphological renal changes in a Göttingen Minipig model of obesity-related and diabetic nephropathy.Scientific reports · 2023Article
- Integrin β1/Cell Surface GRP78 Complex Regulates TGFβ1 and Its Profibrotic Effects in Response to High Glucose.Biomedicines · 2022Article
- suPAR: An Inflammatory Mediator for Kidneys.Kidney diseases (Basel, Switzerland) · 2022Review
- Soluble Urokinase-Type Plasminogen Activator Receptor, Changes of 24-Hour Blood Pressure, and Progression of Chronic Kidney Disease.Journal of the American Heart Association · 2021Observational
- The Predictive Value of Soluble Urokinase-Type Plasminogen Activator Receptor in Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention.International journal of general medicine · 2021Article
- β3-integrin Leu33Pro gain of function variant does not modulate inflammatory activity in human derived macrophages in diabetes.International journal of medical sciences · 2021Observational
- PodocyteFrontiers in pharmacology · 2021Article
- Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- Long-term case study of a Wuzhishan miniature pig with diabetes.Animal models and experimental medicine · 2020Article
- Soluble Urokinase Receptor and Acute Kidney Injury.The New England journal of medicine · 2020Article
- Animal Models of Diabetes-Associated Renal Injury.Journal of diabetes research · 2020Review
- Molecular Imaging of the Glomerulus via Mesangial Cell Uptake of Radiolabeled Tilmanocept.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2019Article
- Emerging strategies to disrupt the central TGF-β axis in kidney fibrosis.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Soluble Urokinase Plasminogen Activator Receptor and Decline in Kidney Function in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2019Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Hyperglycemia stimulates secretion of αVβ3 ligands from vascular cells, including endothelial cells, resulting in activation of the αVβ3 integrin. This study determined whether blocking ligand occupancy of αVβ3 would inhibit the development of diabetic nephropathy. Ten diabetic pigs received an F(ab)2 fragment of an antibody directed against the extracellular domain of the β3-subunit, and 10 received a control IgG F(ab)2 for 18 weeks. Nondiabetic pigs excreted 115 ± 50 μg of protein/mg creatinine compared with control F(ab)2-treated diabetic animals (218 ± 57 μg/mg), whereas diabetic animals treated with the anti-β3 F(ab)2 excreted 119 ± 55 μg/mg (P < .05). Mesangial volume/glomerular volume increased to 21 ± 2.4% in control-treated diabetic animals compared with 14 ± 2.8% (P < .01) in animals treated with active antibody. Diabetic animals treated with control F(ab)2 had significantly less glomerular podocin staining compared with nondiabetic animals, and this decrease was attenuated by treatment with anti-β3 F(ab)2. Glomerular basement membrane thickness was increased in the control, F(ab)2-treated diabetic animals (212 ± 14 nm) compared with nondiabetic animals (170 ± 8.8 nm), but it was unchanged (159.9 ± 16.4 nm) in animals receiving anti-β3 F(ab)2. Podocyte foot process width was greater in control, F(ab)2-treated, animals (502 ± 34 nm) compared with animals treated with the anti-β3 F(ab)2 (357 ± 47 nm, P < .05). Renal β3 tyrosine phosphorylation decreased from 13 934 ± 6437 to 6730 ± 1524 (P < .01) scanning units in the anti-β3-treated group. We conclude that administration of an antibody that inhibits activation of the β3-subunit of αVβ3 that is induced by hyperglycemia attenuates proteinuria and early histologic changes of diabetic nephropathy, suggesting that it may have utility in preventing the progression of this disease complication.
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