ArticleBlood advances2019
Absence of complement component 3 does not prevent classical pathway-mediated hemolysis.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed.
- In vivo evidence of effective complement modulation by TriFu in comparison to C5 inhibition and complement depletion.Blood advances · 2026Article
- A second generation of C3 humanized rats for preclinical evaluation of human C3 inhibitors.Blood vessels, thrombosis & hemostasis · 2026Article
- Reduced C3 Levels Link Dyslipidemia and Renal Involvement in Systemic Lupus Erythematosus.Journal of inflammation research · 2026Article
- Clinical characteristics and management of paroxysmal nocturnal haemoglobinuria in Latin America: a narrative review.Annals of hematology · 2025Review
- Article
- CG001, a C3b-targeted complement inhibitor, blocks 3 complement pathways: development and preclinical evaluation.Blood advances · 2024Article
- Triple-fusion protein (TriFu): A potent, targeted, enzyme-like inhibitor of all three complement activation pathways.The Journal of biological chemistry · 2024Article
- Inflammatory Progression in Patients Undergoing Extracorporeal Membrane Oxygenation.Current molecular medicine · 2024Review
- Surface antibody changes protein corona both in human and mouse serum but not final opsonization and elimination of targeted polymeric nanoparticles.Journal of nanobiotechnology · 2023Article
- Protein therapeutics and their lessons: Expect the unexpected when inhibiting the multi-protein cascade of the complement system.Immunological reviews · 2023Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Complement component 3 (C3) is emerging as a potential therapeutic target. We studied complement-mediated hemolysis using normal and C3-depleted human sera, wild-type (WT) and C3-deficient rat sera, and WT and C3 knockout rat models. In all of the in vitro and in vivo experiments, we found that the loss of C3 did not prevent classical pathway-mediated hemolysis, but it did almost abolish alternative pathway-mediated hemolysis. Experiments using preassembled classical pathway C3 convertases confirmed that C4b2a directly activated complement component 5 (C5), leading to membrane attack complex formation and hemolysis. Our results suggest that targeting C3 should effectively inhibit hemolysis and tissue damage mediated by the alternative pathway of complement activation, but this approach might have limited efficacy in treating classical pathway-mediated pathological conditions.
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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.