ArticleJournal of the American Society of Nephrology : JASN2014
Role of podocyte B7-1 in diabetic nephropathy.
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 77 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 130 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Continuous glucose monitoring in patients with type 2 diabetes on hemodialysis.Acta diabetologica · 2021Pooled it
- Tacrolimus to belatacept conversion in proteinuric kidney transplant recipients.Frontiers in immunology · 2024Trial
- Targeting TFAM K76 acetylation attenuates mitochondrial dysfunction and kidney injury in diabetic kidney disease.Cardiovascular diabetology · 2026Article
- Dissecting causal relationships between immune cells, blood metabolites, and diabetic nephropathy.Diabetology & metabolic syndrome · 2025Article
- New Onset Diabetes After Organ Transplantation: Risk Factors, Treatment, and Consequences.Diagnostics (Basel, Switzerland) · 2025Review
- Article
- sCD163, sCD28, sCD80, and sCTLA-4 as soluble marker candidates for detecting immunosenescence.Immunity & ageing : I & A · 2024Review
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- "Idiopathic" minimal change nephrotic syndrome: a podocyte mystery nears the end.American journal of physiology. Renal physiology · 2023Review
- GLP-1 Receptor Agonist Improves Mitochondrial Energy Status and Attenuates Nephrotoxicity In Vivo and In Vitro.Metabolites · 2023Article
- Urinary CD80 and Serum suPAR as Biomarkers of Glomerular Disease among Adults in Brazil.Diagnostics (Basel, Switzerland) · 2023Article
- Biologics in steroid resistant nephrotic syndrome in childhood: review and new hypothesis-driven treatment.Frontiers in immunology · 2023Review
- State of the art in childhood nephrotic syndrome: concrete discoveries and unmet needs.Frontiers in immunology · 2023Review
- Single-cell RNA and transcriptome sequencing profiles identify immune-associated key genes in the development of diabetic kidney disease.Frontiers in immunology · 2023Article
- B7-1 mediates podocyte injury and glomerulosclerosis through communication with Hsp90ab1-LRP5-β-catenin pathway.Cell death and differentiation · 2022Article
- How immunosuppressive drugs may directly target podocytes in glomerular diseases.Pediatric nephrology (Berlin, Germany) · 2022Review
- Role of the adaptive immune system in diabetic kidney disease.Journal of diabetes investigation · 2022Review
- Thrombomodulin activation driven by LXR agonist attenuates renal injury in diabetic nephropathy.Frontiers in medicine · 2022Article
- Identification of Markers for Diagnosis and Treatment of Diabetic Kidney Disease Based on the Ferroptosis and Immune.Oxidative medicine and cellular longevity · 2022Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors at 13 institutions in 4 countries.
Funding
Abstract
Podocyte injury and resulting albuminuria are hallmarks of diabetic nephropathy, but targeted therapies to halt or prevent these complications are currently not available. Here, we show that the immune-related molecule B7-1/CD80 is a critical mediator of podocyte injury in type 2 diabetic nephropathy. We report the induction of podocyte B7-1 in kidney biopsy specimens from patients with type 2 diabetes. Genetic and epidemiologic studies revealed the association of two single nucleotide polymorphisms at the B7-1 gene with diabetic nephropathy. Furthermore, increased levels of the soluble isoform of the B7-1 ligand CD28 correlated with the progression to ESRD in individuals with type 2 diabetes. In vitro, high glucose conditions prompted the phosphatidylinositol 3 kinase-dependent upregulation of B7-1 in podocytes, and the ectopic expression of B7-1 in podocytes increased apoptosis and induced disruption of the cytoskeleton that were reversed by the B7-1 inhibitor CTLA4-Ig. Podocyte expression of B7-1 was also induced in vivo in two murine models of diabetic nephropathy, and treatment with CTLA4-Ig prevented increased urinary albumin excretion and improved kidney pathology in these animals. Taken together, these results identify B7-1 inhibition as a potential therapeutic strategy for the prevention or treatment of diabetic nephropathy.
Indexed as
Identifiers
What OpenQuestion holds
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.