ArticleKidney international reports2026
Dual Role of Factor H-Related Protein 1 in IgA Nephropathy Kidney Injury.
Article in Kidney international reports, 2026. 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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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
2 citing papers in PubMed.
- Association of Complement Genetics with Outcomes in IgA Nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
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Authors and funding
7 authors.
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Abstract
Introduction: IgA nephropathy (IgAN) is characterized by glomerular IgA deposition, inducing complement activation and inflammation. Previous investigations have highlighted the association of factor H (FH)-related protein 1 (FHR-1) with IgAN. Given the dual functionality of FHR-1, encompassing its "canonical function" in complement activation and "noncanonical function" in triggering inflammation, this study investigated the role of FHR-1 in IgAN-associated kidney injury. Methods: Results: Following pathogenic cIgA1-IC treatment, FHR-1 demonstrated increased binding affinity to mesangial cells. Besides, FHR-1 augmented C3c deposition on mesangial cells. Upon bound to mesangial cells, FHR-1 stimulated cocultured monocytes to secrete higher levels of inflammatory cytokines, interleukin (IL)-1β and IL-18, mediated by complement activation-induced C3a-C3aR and C5a-C5aR pathway activation, and complement-independent interaction with EMR2 on monocytes. In the murine model, intraperitoneally injected FHR-1 heightened glomerular C3 deposition, F4/80+ macrophage, and Ly6G+ neutrophils infiltration, whereas coinjection with FHR-1 Conclusion: FHR-1 exacerbates kidney injury in IgAN by accelerating complement activation and inflammation. FHR-1
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