ArticleJournal of the American Society of Nephrology : JASN2016
B7-1 Is Not Induced in Podocytes of Human and Experimental Diabetic Nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 38 citations in OpenAlex.
- Loss of glomerular aldolase B in diabetic nephropathy promotes renal fibrosis via activating Akt/GSK/β-catenin axis.Journal of advanced research · 2025Article
- Tubular Injury in Diabetic Kidney Disease: Early Diagnosis and Intervention Strategies.Diabetes/metabolism research and reviews · 2025Review
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- Long noncoding RNA ENST00000436340 promotes podocyte injury in diabetic kidney disease by facilitating the association of PTBP1 with RAB3B.Cell death & disease · 2023Article
- T cells and their products in diabetic kidney disease.Frontiers in immunology · 2023Review
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
- B7-1 mediates podocyte injury and glomerulosclerosis through communication with Hsp90ab1-LRP5-β-catenin pathway.Cell death and differentiation · 2022Article
- Losartan Protects Podocytes against High Glucose-induced Injury by Inhibiting B7-1 Expression.Current medical science · 2021Article
- Article
- Urinary CD80 Discriminates Among Glomerular Disease Types and Reflects Disease Activity.Kidney international reports · 2020Article
- [Minimal change disease and focal segmental glomerulosclerosis].Der Internist · 2019Review
- Renal toxicities associated with pembrolizumab.Clinical kidney journal · 2019Article
- The role of B7-1 in proteinuria of glomerular origin.Nature reviews. Nephrology · 2018Review
- Urinary CD80: a biomarker for a favorable response to corticosteroids in minimal change disease.Pediatric nephrology (Berlin, Germany) · 2018Article
- Interaction of CD80 with Neph1: a potential mechanism of podocyte injury.Clinical and experimental nephrology · 2018Article
- Understanding Podocyte Biology to Develop Novel Kidney Therapeutics.Frontiers in endocrinology · 2018Review
- Tubular B7-1 expression parallels proteinuria levels, but not clinical outcomes in adult minimal change disease patients.Scientific reports · 2017Article
- The costimulatory receptor B7-1 is not induced in injured podocytes.Kidney international · 2016Article
- Targeting the podocyte cytoskeleton: from pathogenesis to therapy in proteinuric kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2016Review
- B7-1 Blockade Does Not Improve Post-Transplant Nephrotic Syndrome Caused by Recurrent FSGS.Journal of the American Society of Nephrology : JASN · 2016Article
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7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The incidence of progressive kidney disease associated with diabetes continues to rise worldwide. Current standard therapy with angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers achieves only partial renoprotection, increasing the need for novel therapeutic approaches. Previous studies described B7-1 induction in podocytes of patients with proteinuria, including those with FSGS and type 2 diabetic nephropathy (DN). These findings sparked great excitement in the renal community, implying that abatacept, a costimulatory inhibitor that targets B7-1, could be a novel therapy for diabetic renal disease. Given previous concerns over the value of B7-1 immunostaining and the efficacy of abatacept in patients with recurrent FSGS after renal transplantation, we investigated B7-1 expression in human and experimental DN before embarking on clinical studies of the use of B7-1 targeting strategies to treat proteinuria in DN. Immunohistochemical analysis of kidney specimens using different antibodies revealed that B7-1 is not induced in podocytes of patients with DN, independent of disease stage, or BTBR ob/obmice, a model of type 2 diabetes. These results do not support the use of abatacept as a therapeutic strategy for targeting podocyte B7-1 for the prevention or treatment of DN.
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