ArticleJournal of the American Society of Nephrology : JASN2016
Efficacy of Targeted Complement Inhibition in Experimental C3 Glomerulopathy.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Time to move to a cluster-based management of C3G/IC-MPGN.Pediatric nephrology (Berlin, Germany) · 2026Article
- A novel fusion protein reduces kidney complement in experimental C3 glomerulopathy.Clinical and experimental immunology · 2026Article
- C3d-Targeted factor H inhibits tissue complement in disease models and reduces glomerular injury without affecting circulating complement.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- C3 Glomerulopathy: Novel Treatment Paradigms.Kidney international reports · 2024Review
- Defining Nephritic Factors as Diverse Drivers of Systemic Complement Dysregulation in C3 Glomerulopathy.Kidney international reports · 2024Article
- Therapeutic Potential of Targeting Complement C5a Receptors in Diabetic Kidney Disease.International journal of molecular sciences · 2023Review
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
- Complement activity is regulated in C3 glomerulopathy by IgG-factor H fusion proteins with and without properdin targeting domains.Kidney international · 2021Article
- Homodimeric Minimal Factor H:Frontiers in immunology · 2021Article
- Functional Evaluation of AMD-Associated Risk Variants of Complement Factor B.Investigative ophthalmology & visual science · 2020Article
- Hyperfunctional complement C3 promotes C5-dependent atypical hemolytic uremic syndrome in mice.The Journal of clinical investigation · 2019Article
- Complement Inhibitor CRIg/FH Ameliorates Renal Ischemia Reperfusion Injury via Activation of PI3K/AKT Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Tissue-targeted complement therapeutics.Molecular immunology · 2018Review
- An Engineered Complement Factor H Construct for Treatment of C3 Glomerulopathy.Journal of the American Society of Nephrology : JASN · 2018Article
- The MFHR1 Fusion Protein Is a Novel Synthetic Multitarget Complement Inhibitor with Therapeutic Potential.Journal of the American Society of Nephrology : JASN · 2018Article
- Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways.Kidney international reports · 2016Review
- Distinct roles for the complement regulators factor H and Crry in protection of the kidney from injury.Kidney international · 2016Article
- Biologics for the treatment of autoimmune renal diseases.Nature reviews. Nephrology · 2016Review
- Overview of C3 Glomerulopathy.Frontiers in pediatrics · 2016Review
- Alternative Pathway Dysregulation and the Conundrum of Complement Activation by IgG4 Immune Complexes in Membranous Nephropathy.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
10 authors.
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Abstract
C3 glomerulopathy refers to renal disorders characterized by abnormal accumulation of C3 within the kidney, commonly along the glomerular basement membrane (GBM). C3 glomerulopathy is associated with complement alternative pathway dysregulation, which includes functional defects in complement regulator factor H (FH). There is no effective treatment for C3 glomerulopathy. We investigated the efficacy of a recombinant mouse protein composed of domains from complement receptor 2 (CR2) and FH (CR2-FH) in two models of C3 glomerulopathy with either preexisting or triggered C3 deposition along the GBM. FH-deficient mice spontaneously develop renal pathology associated with abnormal C3 accumulation along the GBM and secondary plasma C3 deficiency. CR2-FH partially restored plasma C3 levels in FH-deficient mice 2 hours after intravenous injection. CR2-FH specifically targeted glomerular C3 deposits, reduced the linear C3 reactivity assessed with anti-C3 and anti-C3b/iC3b/C3c antibodies, and prevented further spontaneous accumulation of C3 fragments along the GBM. Reduction in glomerular C3d and C9/C5b-9 reactivity was observed after daily administration of CR2-FH for 1 week. In a second mouse model with combined deficiency of FH and complement factor I, CR2-FH prevented de novo C3 deposition along the GBM. These data show that CR2-FH protects the GBM from both spontaneous and triggered C3 deposition in vivo and indicate that this approach should be tested in C3 glomerulopathy.
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