Evidence map›Paper›PMID 24709704›Full record

ArticleCells2013

Targeting neutrophil apoptosis for enhancing the resolution of inflammation.

Driss El Kebir, János G Filep

Open access · goldAbstract read
In one paragraph

Article in Cells, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Selenium and Selenoproteins in Neutrophil Functions.Biological trace element research · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Treatment with lipoxin AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  12. Article
  13. Immunomodulation for Tissue Repair and Regeneration.Tissue engineering and regenerative medicine · 2023
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Observational
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

2 authors at 1 institution in 1 country.

Driss El KebirDepartment of Pathology and Cell Biology, University of Montreal and Research Center, Maisonneuve-Rosemont Hospital, 5415 Boulevard de l'Assomption, Montreal, QC H1T 2M4, Canada. delkebirca@yahoo.fr.
János G FilepDepartment of Pathology and Cell Biology, University of Montreal and Research Center, Maisonneuve-Rosemont Hospital, 5415 Boulevard de l'Assomption, Montreal, QC H1T 2M4, Canada. janos.g.filep@umontreal.ca.
Hôpital Maisonneuve-Rosemont · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resolution of acute inflammation is an active process that requires inhibition of further leukocyte recruitment and removal of leukocytes from inflamed sites. Emigrated neutrophils undergo apoptosis before being removed by scavenger macrophages. Recent studies using a variety of gene knockout, transgenic and pharmacological strategies in diverse models of inflammation established neutrophil apoptosis as a critical control point in resolving inflammation. Analysis of death mechanisms revealed distinct features in executing the death program in neutrophils, which can be exploited as targets for controlling the lifespan of neutrophils. Indeed, anti-inflammatory and pro-resolution lipid mediators derived from essential fatty acids, such as lipoxin A4 and resolvin E1, autacoids and proteins, such as annexin A1 and TRAIL, and cyclin-dependent kinase inhibitors, can enhance the resolution of inflammation through induction of neutrophil apoptosis and promoting their removal by efferocytosis. In this review, we discuss recent advances in understanding the molecular basis of these actions, highlighting the potential of therapeutic induction of neutrophil apoptosis for dampening neutrophil-mediated tissue injury and inflammation underlying a variety of diseases.

Identifiers

PMID24709704
PMCPMC3972676
OpenAlexW2110726506

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.