ArticleEMBO molecular medicine2024
Infected erythrocytes and plasma proteomics reveal a specific protein signature of severe malaria.
Article in EMBO molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Is the Association of Granzyme B and the Exported Parasite Hsp70 a Possible Trojan Horse of Severe Malaria?Advances in experimental medicine and biology · 2026Article
- Plasmodium falciparum gene expression signatures and antibody profiling implicate the fikk, phist, and surf multigene families in severe malaria syndromes.The Journal of infection · 2025Article
- Serum Proteomics Reveals Systemic Responses inPathogens (Basel, Switzerland) · 2025Article
- Exploring the Proteomic Landscape of Cochlear Implant Trauma: An iTRAQ-Based Quantitative Analysis Utilizing an Ex Vivo Model.Journal of clinical medicine · 2025Article
- Hemolysis and Its Clinical Implications in Septic Patients with Acute Respiratory Failure.Journal of clinical medicine · 2025Article
- Proteome Profiling of Red Blood Cells from Patients with COPD Links Proteasome Activation with Abnormal Cell Morphology and Function.International journal of chronic obstructive pulmonary disease · 2025Article
Corrections and comments
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Authors and funding
13 authors at 11 institutions in 4 countries.
Funding
Abstract
Cerebral malaria (CM), the most lethal complication of Plasmodium falciparum severe malaria (SM), remains fatal for 15-25% of affected children despite the availability of treatment. P. falciparum infects and multiplies in erythrocytes, contributing to anemia, parasite sequestration, and inflammation. An unbiased proteomic assessment of infected erythrocytes and plasma samples from 24 Beninese children was performed to study the complex mechanisms underlying CM. A significant down-regulation of proteins from the ubiquitin-proteasome pathway and an up-regulation of the erythroid precursor marker transferrin receptor protein 1 (TFRC) were associated with infected erythrocytes from CM patients. At the plasma level, the samples clustered according to clinical presentation. Significantly, increased levels of the 20S proteasome components were associated with SM. Targeted quantification assays confirmed these findings on a larger cohort (n = 340). These findings suggest that parasites causing CM preferentially infect reticulocytes or erythroblasts and alter their maturation. Importantly, the host plasma proteome serves as a specific signature of SM and presents a remarkable opportunity for developing innovative diagnostic and prognostic biomarkers.
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Registered trials
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