Evidence map›Paper›PMID 17050191›Full record

ReviewInternational journal of hematology2006

Mitochondria in neutrophil apoptosis.

B J van Raam, A J Verhoeven, T W Kuijpers

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Immunometabolism of Myeloid-Derived Suppressor Cells: Implications forInternational journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Metabolic substrate utilization in stress-induced immune cells.Intensive care medicine experimental · 2020
    Review
  13. Article
  14. Article
  15. Review
  16. Metabolic regulation of immune responses.Annual review of immunology · 2014
    Review
  17. Review
  18. Review
  19. Article
  20. Article
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

3 authors.

B J van RaamSanquin Research and Landsteiner Laboratory, Department of Blood Cell Research, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
A J Verhoeven
T W Kuijpers

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Central in the regulation of the short life span of neutrophils are their mitochondria. These organelles hardly contribute to the energy status of neutrophils but play a vital role in the apoptotic process. Not only do the mitochondria contain cytotoxic proteins that are released during apoptosis and contribute to caspase activation, but they also act as sensors of the metabolic and redox state of the cell and as scavengers of free Ca2+. The balance of the expression and activity of the proapoptotic and antiapoptotic members of the Bcl-2 family of proteins determines the life span of neutrophils, because these proteins are essential for the formation of a permeability transition pore in the mitochondria and also seem to control the release of Ca2+ from the endoplasmic reticulum and thereby mitochondrial energy metabolism.

Indexed as

AnimalsApoptosisCalciumCaspasesCell Membrane PermeabilityEndoplasmic ReticulumEnzyme ActivationHumansMitochondriaMitochondrial MembranesNeutrophilsProto-Oncogene Proteins c-bcl-2Signal TransductionCalciumCaspasesProto-Oncogene Proteins c-bcl-2

Identifiers

PMID17050191

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.