ArticleFrontiers in immunology2025
Factor H-related 1 and heparan sulfate architecture contribute to complement dysregulation in C3 glomerulopathy.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- C3 glomerulopathy in transplant "like yet unlike native": Pathophysiology, recent advances in therapeutics and evolving paradigms.World journal of transplantation · 2026Review
- Complement Dysregulation in Kidney Diseases: Mechanisms, Biomarkers, and Emerging Targeted Therapies.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Introduction: Dysregulation of the alternative pathway of complement underlies the pathogenesis of C3 glomerulopathy (C3G). Because Factor H (FH) prevents excessive alternative pathway activity while Factor H-related protein 1 (FHR-1) is believed to enhance this response, we investigated the balance between FH and FHR-1 in C3G. Methods: To assess the role of FHR-1 in C3G pathogenicity, we used a multiplex ligation-dependent probe amplification to detect copy number variants in Results: In this study, we confirm that Discussion: Altogether, we show that as renal function declines, a change in the FHR-1:FH ratio combined with changes in heparan sulfate architecture increase complement activity. These findings suggest that complement activity may contribute to the chronic inflammation and progression of renal damage associated with chronic kidney disease.
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Registered trials
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