ArticleKidney international2022
Factor H related proteins modulate complement activation on kidney cells.
Article in Kidney international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Advances in Complement Research: from Pathophysiology to Precision Medicine.Physiology (Bethesda, Md.) · 2026Review
- Association of Complement Genetics with Outcomes in IgA Nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- Complement Dysregulation in Kidney Diseases: Mechanisms, Biomarkers, and Emerging Targeted Therapies.International journal of molecular sciences · 2026Review
- Identification of novel blood-borne soluble binding partners of factor H-related proteins.Scientific reports · 2026Article
- Properdin deficiency or anti-properdin treatment ameliorates disease in the C3 gain-of-function mouse model of atypical haemolytic uraemic syndrome.Frontiers in immunology · 2026Article
- Truncated complement factor H Y402 gene therapy rescues C3 glomerulonephritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Chronic kidney disease enhances alternative pathway activity: a new paradigm.The Journal of clinical investigation · 2025Review
- Targeted Complement Treatments in Glomerulopathies: A Comprehensive Review.Journal of clinical medicine · 2025Review
- Exploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.Antioxidants (Basel, Switzerland) · 2025Review
- Factor H-related 1 and heparan sulfate architecture contribute to complement dysregulation in C3 glomerulopathy.Frontiers in immunology · 2025Article
- A case of non-lupus full-house nephropathy diagnosed by kidney biopsy but observed IgA nephropathy on second biopsy.CEN case reports · 2024Article
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
- New insights into the role of immunity and inflammation in diabetic kidney disease in the omics era.Frontiers in immunology · 2024Review
- Review
- Female but Not Male Mice Deficient in Soluble IgM Are Susceptible to Chemically Induced Glomerular Injury.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Alternative pathway diagnostics.Immunological reviews · 2023Review
- The diagnostic effectiveness of serum sialic acid predicts both qualitative and quantitative prostate cancer in patients with prostate-specific antigen between 4 and 20 ng/mL.Frontiers in endocrinology · 2023Article
- A bibliometric analysis of complement in IgA nephropathy from 1991 to 2022.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
Abstract
Complement activation at a particular location is determined by the balance of activating and inhibitory proteins. Factor H is a key regulator of the alternative pathway of complement, and genetic or acquired impairments in Factor H are associated with glomerular injury. The human Factor H-related proteins (FHRs) comprise a family of five proteins that are structurally related to Factor H. Variations in the genes or expression levels of the FHRs are also associated with glomerular disease, although the mechanisms of glomerular protection/injury are incompletely understood. To explore the role of the FHRs on complement regulation/dysregulation in the kidney, we expressed and purified recombinant murine FHRs (FHRs A, B, C and E). These four distinct FHRs contain binding regions with high amino acid sequence homology to binding regions within Factor H, but we observed different interactions of the FHRs with Factor H binding ligands, including heparin and C3d. There was differential binding of the FHRs to the resident kidney cell types (mesangial, glomerular endothelial, podocytes, and tubular epithelial). All four FHRs caused complement dysregulation on kidney cell surfaces in vitro, although the magnitude of the effect differed among the FHRs and also varied among the different kidney cells. However, only FHR E caused glomerular complement dysregulation when injected in vivo but did not exacerbate injury when injected into mice with ischemic acute kidney injury, an alternative pathway-mediated model. Thus, our experiments demonstrate that the FHRs have unique, and likely context-dependent, effects on the different cell types within the kidney.
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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 Socratic graph.