ArticleFrontiers in immunology2021
Selective Binding of Heparin/Heparan Sulfate Oligosaccharides to Factor H and Factor H-Related Proteins: Therapeutic Potential for C3 Glomerulopathies.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Decoding the Factor H-Related Proteins: Gatekeepers of Complement Dysregulation in AMD.European journal of immunology · 2026Review
- Interactions of dual antiplatelet and anticoagulant with C1q and FH regulate complement activation by injured cells.Blood vessels, thrombosis & hemostasis · 2026Article
- Glycoinformatic Profiling of Label-Free Intact Heparan Sulfate Oligosaccharides.Molecular & cellular proteomics : MCP · 2026Article
- Identification of novel blood-borne soluble binding partners of factor H-related proteins.Scientific reports · 2026Article
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- Glycosaminoglycans as Polyelectrolytes: Charge, Interactions, and Applications.Chembiochem : a European journal of chemical biology · 2025Review
- Spatially resolved transcriptomic profiling for glomerular and tubulointerstitial gene expression in C3 glomerulopathy.Clinical kidney journal · 2025Article
- Factor H-related 1 and heparan sulfate architecture contribute to complement dysregulation in C3 glomerulopathy.Frontiers in immunology · 2025Article
- Effective long-term treatment with moss-produced factor H by overcoming the antibody response in a mouse model of C3G.Frontiers in immunology · 2025Article
- Defining Nephritic Factors as Diverse Drivers of Systemic Complement Dysregulation in C3 Glomerulopathy.Kidney international reports · 2024Article
- VSIG4 interaction with heparan sulfates inhibits VSIG4-complement binding.Glycobiology · 2023Article
- C3 glomerulopathy: Understanding an ultra-rare complement-mediated renal disease.American journal of medical genetics. Part C, Seminars in medical genetics · 2022Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Complement dysregulation is characteristic of the renal diseases atypical hemolytic uremic syndrome (aHUS) and complement component 3 glomerulopathy (C3G). Complement regulatory protein Factor H (FH) inhibits complement activity, whereas FH-related proteins (FHRs) lack a complement regulatory domain. FH and FHRs compete for binding to host cell glycans, in particular heparan sulfates (HS). HS is a glycosaminoglycan with an immense structural variability, where distinct sulfation patterns mediate specific binding of proteins. Mutations in FH, FHRs, or an altered glomerular HS structure may disturb the FH : FHRs balance on glomerular endothelial cells, thereby leading to complement activation and the subsequent development of aHUS/C3G. In this study, we aimed to identify specific HS structures that could specifically compete off FHRs from HS glycocalyx (HS
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