ReviewSeminars in nephrology2018
Aberrant Glycosylation of the IgA1 Molecule in IgA Nephropathy.
Review in Seminars in nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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.
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Who cites it
55 citing papers in PubMed, 99 citations in OpenAlex.
- Large glycomics datasets as a tool to understand the function of glycans.Nature chemical biology · 2026Review
- Bovine Lactoferrin Modulates Mononuclear Cell Activity in Human Palatine Tonsils.International journal of molecular sciences · 2026Article
- Gene modification: Exploring the potential in treating kidney diseases.Pharmacological research · 2026Review
- Article
- IgA nephropathy: a novel pathway in immunopathogenesis dependent on the timing of Epstein-Barr virus infection.Frontiers in immunology · 2026Review
- Endoplasmic reticulum stress in Hashimoto's thyroiditis: a candidate amplification node linking thyroid-specific vulnerability and immune dysregulation.Frontiers in immunology · 2026Review
- Article
- Transcriptomic Signatures in IgA Nephropathy: From Renal Tissue to Precision Risk Stratification.International journal of molecular sciences · 2025Review
- Proteomic Analysis of Circulating IgA1-Containing Immune Complexes in Patients with IgA Nephropathy.Kidney international reports · 2025Article
- SOCS1 improves abnormal IgA galactosylation in IgA nephropathy by regulating the TLR9/MyD88 pathway.Immunologic research · 2025Article
- Lysosome-mediated aggregation of galactose-deficient IgA1 with transferrin receptor 1 links to IgA nephropathy.Nature communications · 2025Article
- The Role of Glycans in Human Immunity-A Sweet Code.Molecules (Basel, Switzerland) · 2025Review
- A Bacteroides thetaiotaomicron genetic locus encodes activities consistent with mucin O-glycoprotein processing and N-acetylgalactosamine metabolism.Nature communications · 2025Article
- Case report: a rare concurrence of dense deposit disease in an adolescent patient with IgA nephropathy.BMC pediatrics · 2025Article
- Lactobacillus casei Cell Wall Extract and Production of Galactose-Deficient IgA1 in a Humanized IGHA1 Mouse Model.Journal of the American Society of Nephrology : JASN · 2025Article
- Biomarker understanding first lessons from drug development for IgA-driven autoimmune and fibrotic diseases.Cambridge prisms. Precision medicine · 2025Review
- The role of antibody glycosylation in autoimmune and alloimmune kidney diseases.Nature reviews. Nephrology · 2024Review
- O-glycosylation of IgA1 and the pathogenesis of an autoimmune disease IgA nephropathy.Glycobiology · 2024Review
- My lifetime in IgA nephropathy: An unexpected journey.Nephrology (Carlton, Vic.) · 2024Article
- Stability Engineering of Recombinant Secretory IgA.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
IgA nephropathy, the most common primary glomerulonephritis in the world and a frequent cause of end-stage renal disease, is characterized by typical mesangial deposits of IgA1, as described by Berger and Hinglaise in 1968. Since then, it has been discovered that aberrant IgA1 O-glycosylation is involved in disease pathogenesis. Progress in glycomic, genomic, clinical, analytical, and biochemical studies has shown autoimmune features of IgA nephropathy. The autoimmune character of the disease is explained by a multihit pathogenesis model, wherein overproduction of aberrantly glycosylated IgA1, galactose-deficient in some O-glycans, by IgA1-secreting cells leads to increased levels of circulatory galactose-deficient IgA1. These glycoforms induce production of autoantibodies that subsequently bind hinge-region of galactose-deficient IgA1 molecules, resulting in the formation of nephritogenic immune complexes. Some of these complexes deposit in the kidney, activate mesangial cells, and incite glomerular injury. Thus, galactose-deficient IgA1 is central to the disease process. In this article, we review studies concerning IgA1 O-glycosylation that have contributed to the current understanding of the role of IgA1 in the pathogenesis of IgA 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.