ArticleNature communications2016
Oxidative insult can induce malaria-protective trait of sickle and fetal erythrocytes.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 56 citations in OpenAlex.
- Phenotypic screens reveal Plasmodium falciparum genetic factors associated with infection of sickle-trait cells.Blood cells, molecules & diseases · 2025Article
- Contact Dynamics of CytoadheringACS infectious diseases · 2025Article
- Whole Blood Transcriptome Analysis in Congenital Anemia Patients.International journal of molecular sciences · 2024Article
- Article
- Influence of the sickle cell trait on Plasmodium falciparum infectivity from naturally infected gametocyte carriers.BMC infectious diseases · 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
- Does fetal hemoglobin inhibit the malarial parasite Plasmodium falciparum?American journal of hematology · 2022Article
- Menadione: a platform and a target to valuable compounds synthesis.Beilstein journal of organic chemistry · 2022Review
- PfEMP1-Specific Immunoglobulin G Reactivity Among Beninese Pregnant Women With Sickle Cell Trait.Open forum infectious diseases · 2021Article
- Sickle Cell Anemia andPathogens (Basel, Switzerland) · 2021Review
- Impact of Sickle Cell Trait Hemoglobin on the Intraerythrocytic Transcriptional Program of Plasmodium falciparum.mSphere · 2021Article
- Functionalized supported membranes for quantifying adhesion of P. falciparum-infected erythrocytes.Biophysical journal · 2021Article
- The apicoplast link to fever-survival and artemisinin-resistance in the malaria parasite.Nature communications · 2021Article
- Sickle-trait hemoglobin reduces adhesion to both CD36 and EPCR by Plasmodium falciparum-infected erythrocytes.PLoS pathogens · 2021Article
- Red blood cell mannoses as phagocytic ligands mediating both sickle cell anaemia and malaria resistance.Nature communications · 2021Article
- Sickle Cell Trait Modulates the Proteome and Phosphoproteome ofFrontiers in cellular and infection microbiology · 2021Article
- Targeting Host Glycolysis as a Strategy for Antimalarial Development.Frontiers in cellular and infection microbiology · 2021Article
- Host Cytoskeleton Remodeling throughout the Blood Stages of Plasmodium falciparum.Microbiology and molecular biology reviews : MMBR · 2019Review
- Review
- Born to sweet delight: Using natural models of malaria protection to understand and neutralize P. falciparum pathogenesis.PLoS pathogens · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasmodium falciparum infections can cause severe malaria, but not every infected person develops life-threatening complications. In particular, carriers of the structural haemoglobinopathies S and C and infants are protected from severe disease. Protection is associated with impaired parasite-induced host actin reorganization, required for vesicular trafficking of parasite-encoded adhesins, and reduced cytoadherence of parasitized erythrocytes in the microvasculature. Here we show that aberrant host actin remodelling and the ensuing reduced cytoadherence result from a redox imbalance inherent to haemoglobinopathic and fetal erythrocytes. We further show that a transient oxidative insult to wild-type erythrocytes before infection with P. falciparum induces the phenotypic features associated with the protective trait of haemoglobinopathic and fetal erythrocytes. Moreover, pretreatment of mice with the pro-oxidative nutritional supplement menadione mitigate the development of experimental cerebral malaria. Our results identify redox imbalance as a causative principle of protection from severe malaria, which might inspire host-directed intervention strategies.
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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 OpenQuestion graph.