ArticleKidney international2017
C5 inhibition prevents renal failure in a mouse model of lethal C3 glomerulopathy.
Article in Kidney international, 2017. 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, 32 citations in OpenAlex.
- The Influence of Anti-C3aR and Anti-C5aR Antibody Levels on the Course of Specific Glomerulonephritis Types.Journal of clinical medicine · 2025Article
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Seventy Years Later: Systemic and Local Properdin in Atherosclerosis.Journal of the American Heart Association · 2025Article
- Improved therapeutic efficacy of a bifunctional anti-C5 mAb-FH SCR1-5 fusion protein over anti-C5 mAb in an accelerated mouse model of C3 glomerulopathy.ImmunoHorizons · 2025Article
- A link between circulating immune complexes and acute kidney injury in human visceral leishmaniasis.Scientific reports · 2024Article
- Immune-Modulating Effects of Low-Carbohydrate Ketogenic Foods in Healthy Canines.Current developments in nutrition · 2024Article
- Alternative Complement Pathway Inhibition With Iptacopan for the Treatment of C3 Glomerulopathy-Study Design of the APPEAR-C3G Trial.Kidney international reports · 2022Article
- The Increase in Circulating Levels of Pro-Inflammatory Chemokines, Cytokines, and Complement C5 in Canines with Impaired Kidney Function.Current issues in molecular biology · 2022Article
- Advances in pediatric acute kidney injury.Pediatric research · 2022Review
- Immunity, endothelial injury and complement-induced coagulopathy in COVID-19.Nature reviews. Nephrology · 2021Review
- Deposition of the Membrane Attack Complex in Healthy and Diseased Human Kidneys.Frontiers in immunology · 2020Review
- Treatment of Rare Inflammatory Kidney Diseases: Drugs Targeting the Terminal Complement Pathway.Frontiers in immunology · 2020Review
- The Pathogenesis of Sepsis and Potential Therapeutic Targets.International journal of molecular sciences · 2019Review
- The role of properdin in complement-mediated renal diseases: a new player in complement-inhibiting therapy?Pediatric nephrology (Berlin, Germany) · 2019Article
- Differential contribution of C5aR and C5b-9 pathways to renal thrombic microangiopathy and macrovascular thrombosis in mice carrying an atypical hemolytic syndrome-related factor H mutation.Kidney international · 2019Article
- Complement Factor H Mutation W1206R Causes Retinal Thrombosis and Ischemic Retinopathy in Mice.The American journal of pathology · 2019Article
- Prevention of Fatal C3 Glomerulopathy by Recombinant Complement Receptor of the Ig Superfamily.Journal of the American Society of Nephrology : JASN · 2018Article
- Retinal Basal Laminar Deposits in Complement fH/fP Mouse Model of Dense Deposit Disease.Investigative ophthalmology & visual science · 2018Article
- Blocking Properdin Prevents Complement-Mediated Hemolytic Uremic Syndrome and Systemic Thrombophilia.Journal of the American Society of Nephrology : JASN · 2018Article
- Mechanically induced CaBone research · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
C3 glomerulopathy is a potentially life-threatening disease of the kidney caused by dysregulated alternative pathway complement activation. The specific complement mediator(s) responsible for kidney injury in C3 glomerulopathy are yet to be defined and no specific therapy is currently available. We previously developed a mouse model of lethal C3 glomerulopathy with factor H and properdin gene double mutations. Therefore, we used this model to examine the role of C5 and C5a receptor (C5aR) in the pathogenesis of the disease. Disease severity in these factor H/properdin double-mutant mice was found to be correlated with plasma C5 levels, and prophylactic anti-C5 mAb therapy was effective in preventing lethal C3 glomerulopathy. When given to these double-mutant mice that had already developed active disease with severe proteinuria, anti-C5 mAb treatment also prevented death in half of the mice. Deficiency of C5aR significantly reduced disease severity, suggesting that C5aR-mediated inflammation contributed to C3 glomerulopathy. Thus, C5 and C5aR have a critical role in C3 glomerulopathy. Hence, early intervention targeting these pathways may be an effective therapeutic strategy for patients with C3 glomerulopathy.
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