ArticleFrontiers in immunology2020
Hemoglobin Genotypes Modulate Inflammatory Response to
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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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
13 citing papers in PubMed, 14 citations in OpenAlex.
- Genetic variants in red blood cell adhesion-related genes influence the severity of sickle cell anemia in a malaria-endemic region : Short title: Genetic variants in red blood cell adhesion-related genes in sickle cell anemia.Molecular biology reports · 2026Article
- Distinct systemic cytokine signatures define symptomatic malaria in children: insights from a longitudinal study in Togo.BMC infectious diseases · 2026Article
- Human genetic variations conferring resistance to malaria.Journal of translational medicine · 2025Review
- Circulating biomarkers associated with pediatric sickle cell disease.Frontiers in molecular biosciences · 2024Article
- Modulation of Heme-Induced Inflammation Using MicroRNA-Loaded Liposomes: Implications for Hemolytic Disorders Such as Malaria and Sickle Cell Disease.International journal of molecular sciences · 2023Article
- Differences in the distribution of hemoglobin variants according to the geographic regions in a Colombian population.Hematology, transfusion and cell therapy · 2023Article
- Pattern of admissions and outcome in the children emergency department of a tertiary health institution in Southwestern Nigeria: A four-year review.African journal of emergency medicine : Revue africaine de la medecine d'urgence · 2023Article
- Sickle Cell Hemoglobin Genotypes Affect Malaria Parasite Growth and Correlate with Exosomal miR-451a and let-7i-5p Levels.International journal of molecular sciences · 2023Article
- Infrastructure for bioinformatics applications in Tanzania: Lessons from the Sickle Cell Programme.PLoS computational biology · 2023Article
- Early Prediction of Epilepsy after Encephalitis in Childhood Based on EEG and Clinical Features.Emergency medicine international · 2023Article
- MicroRNAs miR-451a and Let-7i-5p Profiles in Circulating Exosomes Vary among Individuals with Different Sickle Hemoglobin Genotypes and Malaria.Journal of clinical medicine · 2022Article
- MiR-451a and let-7i-5p loaded extracellular vesicles attenuate heme-induced inflammation in hiPSC-derived endothelial cells.Frontiers in immunology · 2022Article
- Analysis of clinical presentation, hematological factors, self-reported bed net usage, and malaria burden in sickle cell disease patients.EClinicalMedicine · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
In 2018, 228 million cases and 405,000 malaria-associated deaths were reported worldwide with a majority being in Africa. A wide range of factors, including parasitemia, host immunity, inflammatory responses to infection, and host hemoglobin genotype, mediate the severity of malaria. Among the hemoglobinopathies, hemoglobin S (HbS) is caused by a single amino acid substitution of Glutamic Acid replaced by Valine at the sixth position of the beta-globin chain (E6V). Hemoglobin C (HbC) on the other hand, involves a single amino acid substitution of Glutamic Acid by a Lysine (E6K), which has received the most attention. These substitutions alter the stability of Hb leading to wide-ranging hematological disorders. The homozygous state of hemoglobin S (HbSS) results in sickle cell anemia (SCA) whereas the heterozygous state (HbAS) results in sickle cell trait (SCT). Both mutations are reported to mediate the reduction in the severity and fatality of
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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.