ArticleJournal of the American Society of Nephrology : JASN2012
Fcγ receptor deficiency attenuates diabetic nephropathy.
Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.
- Optimizing diabetic kidney disease animal models: Insights from a meta-analytic approach.Animal models and experimental medicine · 2023Pooled it
- Glycosylation Profile of IgG in Moderate Kidney Dysfunction.Journal of the American Society of Nephrology : JASN · 2016Pooled it
- Monoclonal antibodies associated IgA nephropathy or other nephropathies.Frontiers in pharmacology · 2026Review
- Targeting NF-κB in diabetic nephropathy: exploring the therapeutic potential of phytoconstituents.Archives of pharmacal research · 2025Review
- Comparison of genetic and epigenetic profiles of periodontitis according to the presence of type 2 diabetes.MedComm · 2024Article
- Store-operated CaExperimental biology and medicine (Maywood, N.J.) · 2023Review
- Fcα Receptor Type I and Its Association with Atherosclerosis Development.Juntendo Iji zasshi = Juntendo medical journal · 2023Article
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
- Fcγ receptor activation mediates vascular inflammation and abdominal aortic aneurysm development.Clinical and translational medicine · 2021Article
- Identification of Hub Genes Associated with Hypertension and Their Interaction with miRNA Based on Weighted Gene Coexpression Network Analysis (WGCNA) Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- The varying roles of macrophages in kidney injury and repair.Current opinion in nephrology and hypertension · 2020Review
- Association of the IgGBMJ open diabetes research & care · 2020Article
- Macrophages: versatile players in renal inflammation and fibrosis.Nature reviews. Nephrology · 2019Review
- An Inflammatory Story: Antibodies in Tuberculosis Comorbidities.Frontiers in immunology · 2019Review
- FcgRIII Deficiency and FcgRIIb Defeciency Promote Renal Injury in Diabetic Mice.BioMed research international · 2019Article
- Role of the Immune System in Diabetic Kidney Disease.Current diabetes reports · 2018Review
- Non-genetic mechanisms of diabetic nephropathy.Frontiers of medicine · 2017Review
- TWEAK blockade decreases atherosclerotic lesion size and progression through suppression of STAT1 signaling in diabetic mice.Scientific reports · 2017Article
- Suppressor of Cytokine Signaling-1 Peptidomimetic Limits Progression of Diabetic Nephropathy.Journal of the American Society of Nephrology : JASN · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among patients with diabetes, increased production of immunoglobulins against proteins modified by diabetes is associated with proteinuria and cardiovascular risk, suggesting that immune mechanisms may contribute to the development of diabetes complications, such as nephropathy. We investigated the contribution of IgG Fcγ receptors to diabetic renal injury in hyperglycemic, hypercholesterolemic mice. We used streptozotocin to induce diabetes in apolipoprotein E-deficient mice and in mice deficient in both apolipoprotein E and γ-chain, the common subunit of activating Fcγ receptors. After 15 weeks, the mice lacking Fcγ receptors had significantly less albuminuria and renal hypertrophy, despite similar degrees of hyperglycemia and hypercholesterolemia, immunoglobulin production, and glomerular immune deposits. Moreover, diabetic Fcγ receptor-deficient mice had less mesangial matrix expansion, inflammatory cell infiltration, and collagen and α-smooth muscle actin content in their kidneys. Accordingly, expression of genes involved in leukocyte infiltration, fibrosis, and oxidative stress was significantly reduced in diabetic kidneys and in mesangial cells cultured from Fcγ receptor-deficient mice. In summary, preventing the activation of Fcγ receptors alleviates renal hypertrophy, inflammation, and fibrosis in hypercholesterolemic mice with diabetes, suggesting that modulating Fcγ receptor signaling may be renoprotective in diabetic nephropathy.
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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.