Evidence map›Paper›PMID 30291189›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Glucose metabolism mediates disease tolerance in cerebral malaria.

Andrew Wang, Sarah C Huen, Harding H Luan, Kelly Baker, Henry Rinder, Carmen J Booth, Ruslan Medzhitov

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
10.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
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  7. Evolution of the ocular immune system.Eye (London, England) · 2025
    Review
  8. UHPLC/MS Profile and Antimalarial Potency ofAdvances in pharmacological and pharmaceutical sciences · 2025
    Article
  9. Review
  10. The intersection of hostMicrobiology and molecular biology reviews : MMBR · 2024
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Andrew WangRheumatology Unit, Department of Medicine, Yale University School of Medicine, New Haven, CT 06520.
Sarah C HuenNephrology Unit, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Harding H LuanDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520.
Kelly BakerDepartment of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520.
Henry RinderDepartment of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520.
Carmen J BoothDepartment of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520.
Ruslan MedzhitovDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; ruslan.medzhitov@yale.edu.ORCID 0000-0002-7021-2012
Yale University · USHoward Hughes Medical Institute · USThe University of Texas Southwestern Medical Center · US

Funding

TRAINING PROGRAM IN INVESTIGATIVE RHEUMATOLOGYT32AR007107 · NIAMS · YALE UNIVERSITY · PI RICHARD J BUCALA · 1986 to 2026
$7.5M
The Role of Kidney FGF21 in Surviving SepsisK08DK110424 · NIDDK · YALE UNIVERSITY · PI HUEN, SARAH · 2016 to 2020
$833k
Regulation of Metabolic Programs for Host Tolerance to InflammationK08AI128745 · NIAID · YALE UNIVERSITY · PI WANG, ANDREW · 2017 to 2021
$784k
NIAID NIH HHS K08 AI128745NIAMS NIH HHS T32 AR007107NIDDK NIH HHS K08 DK110424
6 · The paper itself

Abstract

Sickness behaviors are a conserved set of stereotypic responses to inflammatory diseases. We recently demonstrated that interfering with inflammation-induced anorexia led to metabolic changes that had profound effects on survival of acute inflammatory conditions. We found that different inflammatory states needed to be coordinated with corresponding metabolic programs to actuate tissue-protective mechanisms. Survival of viral inflammation required intact glucose utilization pathways, whereas survival of bacterial inflammation required alternative fuel substrates and ketogenic programs. We thus hypothesized that organismal metabolism would be important in other classes of infectious inflammation and sought to understand its role in the prototypic parasitic disease malaria. Utilizing the cerebral malaria model,

Indexed as

AnimalsBlood-Brain BarrierBrainDisease Models, AnimalGlucoseImmune ToleranceInflammationMalaria, CerebralMaleMiceMice, Inbred C57BLParasitemiaPlasmodium bergheiGlucoseinflammationmalariametabolism

Identifiers

PMID30291189
PMCPMC6205430
OpenAlexW2894989586

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.