Evidence map›Paper›PMID 17029647›Full record

ReviewMalaria journal2006

Human malarial disease: a consequence of inflammatory cytokine release.

Ian A Clark, Alison C Budd, Lisa M Alleva, William B Cowden

Open access · goldAbstract readReview
In one paragraph

Review in Malaria journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 4 pooled it
12.6field-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

140 citing papers in PubMed, 4 syntheses or guidelines pooled it, 307 citations in OpenAlex.

  1. Pooled it
  2. Low Interleukin-12 Levels concerning Severe Malaria: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2022
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. A Balanced Proinflammatory and Regulatory Cytokine Signature in Young African Children Is Associated With Lower Risk of Clinical Malaria.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2019
    Trial
  7. Trial
  8. Review
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Infection and immunity · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

80 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Ian A ClarkSchool of Biochemistry and Molecular Biology, Australian National University, Canberra, ACT 0200, Australia. ian.clark@anu.edu.au
Alison C Budd
Lisa M Alleva
William B Cowden
Australian National University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficiency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease.

Indexed as

CytokinesHumansInflammationMalariaCytokines

Identifiers

PMID17029647
PMCPMC1629020
OpenAlexW2167223311

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.