ArticleProceedings of the National Academy of Sciences of the United States of America2019
P-selectin drives complement attack on endothelium during intravascular hemolysis in TLR-4/heme-dependent manner.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05062486 (An Open-Label, Randomized, Double Arm, Phase 2 Study to Evaluate the Safety and Efficacy of C and RQC for Preventing Progression in Age-Related Macular Degeneration), which is not on this map. Cited by 81 papers.
What it found
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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.
The trial behind it
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.
An Open-Label, Randomized, Double Arm, Phase 2 Study to Evaluate the Safety and Efficacy of C and RQC for Preventing Progression in Age-Related Macular Degeneration
Who cites it
81 citing papers in PubMed, 110 citations in OpenAlex.
- Comprehensive analysis of complement activation in a hydroxyurea-treated patient cohort with sickle cell disease.Blood advances · 2026Article
- Examination of Antigen-Specific B Cell Responses to Red Blood Cell Transfusion.Methods in molecular biology (Clifton, N.J.) · 2026Article
- The Immunology of Transfusion Medicine: Past, Present, and Future.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Analysis of Biotinylated Red Blood Cells Following Transfusion.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Analysis of Erythrocyte Membrane Alloantigens.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Acute Incompatible Red Blood Cell Transfusion in Mice.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Flow Cytometric Examination of Galectin Binding to Red Blood Cells.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Determining the Binding Affinity in Monoclonal Antibody-Alloantigen Interactions.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Modeling antithymocyte globulin-induced microvasculopathy using human iPSC-derived vascularized liver organoids.Cell reports. Medicine · 2025Article
- HCAR2 is a novel receptor for heme.Blood advances · 2025Article
- The role of complement in long COVID pathogenesis.JCI insight · 2025Review
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Complement is activated in patients with acute chest syndrome caused by sickle cell disease and represents a therapeutic target.Science translational medicine · 2025Article
- Cryo-EM analysis of complement C3 reveals a reversible major opening of the macroglobulin ring.Nature structural & molecular biology · 2025Article
- Transcriptomic atlas reveals organ-specific disease tolerance in sickle cell mice.Blood advances · 2025Article
- CD47 regulates antigen modulation and red blood cell clearance following an incompatible transfusion.Frontiers in immunology · 2025Article
- P-Selectin, Vascular Endothelial Cadherin, and Vascular Cell Adhesion Molecule-1 as Novel Biomarkers for ABO Hemolytic Disease of the Fetus and Newborn.Analytical cellular pathology (Amsterdam) · 2025Article
- Thrombotic Microangiopathy as an Emerging Complication of Viral Vector-Based Gene Therapy.Kidney international reports · 2024Review
- Prevalence and predictors of iron deficiency anaemia among children with sickle cell disease in Dodoma, Tanzania: a cross-sectional study.BMC public health · 2024Article
- A guide to complement biology, pathology and therapeutic opportunity.Nature reviews. Immunology · 2024Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemolytic diseases are frequently linked to multiorgan failure subsequent to vascular damage. Deciphering the mechanisms leading to organ injury upon hemolytic event could bring out therapeutic approaches. Complement system activation occurs in hemolytic disorders, such as sickle cell disease, but the pathological relevance and the acquisition of a complement-activating phenotype during hemolysis remain unclear. Here we found that intravascular hemolysis, induced by injection of phenylhydrazine, resulted in increased alanine aminotransferase plasma levels and NGAL expression. This liver damage was at least in part complement-dependent, since it was attenuated in complement C3
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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 OpenQuestion graph.