ArticleFrontiers in immunology2022
Heme Interferes With Complement Factor I-Dependent Regulation by Enhancing Alternative Pathway Activation.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Postpartum Atypical Hemolytic Uremic Syndrome Complicating β-Thalassemia Intermedia: A Case Report and Literature Review.Journal of clinical medicine · 2026Article
- Implantation of a Continuous-Flow Left Ventricular Assist Device During Cardiopulmonary Bypass Is Associated with a Significant and Transient Acute Thromboinflammatory Response.International journal of molecular sciences · 2026Article
- 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
- Proteins of the SubB family provide multiple mechanisms of serum resistance inEmerging microbes & infections · 2025Article
- Complement is activated in patients with acute chest syndrome caused by sickle cell disease and represents a therapeutic target.Science translational medicine · 2025Article
- Current understanding of eryptosis: mechanisms, physiological functions, role in disease, pharmacological applications, and nomenclature recommendations.Cell death & disease · 2025Review
- CD47 regulates antigen modulation and red blood cell clearance following an incompatible transfusion.Frontiers in immunology · 2025Article
- Inhibition of Complement Will Substantially Reduce the Anemia of Malaria.Journal of immunology research · 2025Review
- Case Report: Possible C3 nephritic factor-driven complement-mediated severe hemolytic anemia and acute kidney injury in a child withFrontiers in immunology · 2025Article
- The Neural Palette of Heme: Altered Heme Homeostasis Underlies Defective Neurotransmission, Increased Oxidative Stress, and Disease Pathogenesis.Antioxidants (Basel, Switzerland) · 2024Review
- A guide to complement biology, pathology and therapeutic opportunity.Nature reviews. Immunology · 2024Review
- Review
- Heme Interactions as Regulators of the Alternative Pathway Complement Responses and Implications for Heme-Associated Pathologies.Current issues in molecular biology · 2023Review
- Metalloporphyrins as Tools for Deciphering the Role of Heme Oxygenase in Renal Immune Injury.International journal of molecular sciences · 2023Review
- Functional evaluation of complement factor I variants by immunoassays and SDS-PAGE.Frontiers in immunology · 2023Article
- Liver Disease and Sickle Cell Disease: Auto-Immune Hepatitis more than a Coincidence; A Systematic Review of the Literature.Mediterranean journal of hematology and infectious diseases · 2023Review
- Double-edged functions of hemopexin in hematological related diseases: from basic mechanisms to clinical application.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemolysis, as a result of disease or exposure to biomaterials, is characterized by excess amounts of cell-free heme intravascularly and consumption of the protective heme-scavenger proteins in plasma. The liberation of heme has been linked to the activation of inflammatory systems, including the complement system, through alternative pathway activation. Here, we investigated the impact of heme on the regulatory function of the complement system. Heme dose-dependently inhibited factor I-mediated degradation of soluble and surface-bound C3b, when incubated in plasma or buffer with complement regulatory proteins. Inhibition occurred with factor H and soluble complement receptor 1 as co-factors, and the mechanism was linked to the direct heme-interaction with factor I. The heme-scavenger protein hemopexin was the main contaminant in purified factor I preparations. This led us to identify that hemopexin formed a complex with factor I in normal human plasma. These complexes were significantly reduced during acute vasoocclusive pain crisis in patients with sickle cell disease, but the complexes were normalized at their baseline outpatient clinic visit. Hemopexin exposed a protective function of factor I activity
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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.