ReviewClinical and experimental nephrology2008
Pathogenetic significance of aberrant glycosylation of IgA1 in IgA nephropathy.
Review in Clinical and experimental nephrology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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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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
19 citing papers in PubMed, 38 citations in OpenAlex.
- Inhibition of p65 NF-κB enhances production of galactose-deficient IgA1 through suppression ofbioRxiv : the preprint server for biology · 2026Article
- Review
- Roles ofFrontiers in microbiology · 2024Review
- IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease.Frontiers in immunology · 2023Review
- Aberrantly Glycosylated IgA1 in IgA Nephropathy: What We Know and What We Don't Know.Journal of clinical medicine · 2021Review
- Changes E3 ubiquitin protein ligase 1 gene mRNA expression correlated with IgA1 glycosylation in patients with IgA nephropathy.Renal failure · 2019Article
- Renal expression of trefoil factor 3 mRNA in association with tubulointerstitial fibrosis in IgA nephropathy.Nephrology (Carlton, Vic.) · 2018Article
- Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis.BBA clinical · 2016Article
- Distribution of Streptococcus mutans strains with collagen-binding proteins in the oral cavity of IgA nephropathy patients.Clinical and experimental nephrology · 2015Article
- DNA methylation in Cosmc promoter region and aberrantly glycosylated IgA1 associated with pediatric IgA nephropathy.PloS one · 2015Article
- Serum galactose-deficient IgA1 levels in children with IgA nephropathy.International journal of clinical and experimental medicine · 2015Article
- Mycophenolic acid reverses IgA1 aberrant glycosylation through up-regulating Cosmc expression in IgA nephropathy.International urology and nephrology · 2013Article
- CpG array analysis of histone H3 lysine 4 trimethylation by chromatin immunoprecipitation linked to microarrays analysis in peripheral blood mononuclear cells of IgA nephropathy patients.Yonsei medical journal · 2012Article
- Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.The Journal of clinical investigation · 2011Article
- Genetics and immunopathogenesis of IgA nephropathy.Clinical reviews in allergy & immunology · 2011Review
- Aberrantly glycosylated IgA1 as a factor in the pathogenesis of IgA nephropathy.Clinical & developmental immunology · 2011Review
- Solid-phase synthesis of a pentavalent GalNAc-containing glycopeptide (Tn antigen) representing the nephropathy-associated IgA hinge region.Carbohydrate research · 2010Article
- O-linked oligosaccharides of the IgA1 hinge region: roles of its aberrant structure in the occurrence and/or progression of IgA nephropathy.Clinical and experimental nephrology · 2009Review
- n-3 polyunsaturated fatty acids and autoimmune-mediated glomerulonephritis.Prostaglandins, leukotrienes, and essential fatty acidsReview
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IgA nephropathy (IgAN), the most common form of primary glomerulonephritis worldwide, is defined by predominant IgA1 deposits in the glomerular mesangium. Among abnormalities of the IgA immune system reported so far in IgAN, aberrant O-linked glycosylation in the hinge region of IgA1 is the most consistent finding. IgA1 molecules bearing abnormal glycosylation have been found in serum, in tonsillar lymphocytes, and in eluate from mesangial deposits, and characterized by decreased O-linked N-acetylgalactosamine residues with or without alteration in the terminal sialylation of the O-linked sugars. IgA1 with incomplete galactosylation has a tendency to accumulate in glomerular mesangium by self-aggregation or immune complex formation. Glomerular mesangial cells exposed to immune complexes of these IgA1 can proliferate and secrete cytokines, chemokines, growth factors, and extracellular matrix components promoting inflammatory reactions in the glomeruli. Although genes encoding enzymes involved in the O-glycosylation process, such as C1GALT1, have been reported to be responsible for susceptibility to IgAN, recent evidence suggests that the abnormality is restricted to a small fraction of B cell populations and arises from dysregulated IgA1 production and secretion in mucosal immune system. This review will focus on and discuss the role of incompleteness of IgA1 O-galactosylation in the pathogenesis of IgAN and propose a possible mechanism in which abnormal IgA1 occurs in IgAN.
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