Evidence map›Paper›PMID 26248079›Full record

ReviewToxins2015

Interactions between Autophagy and Bacterial Toxins: Targets for Therapy?

Jacques Mathieu

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Macrophage LC3-associated phagocytosis is an immune defense againstProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. The functions of azurin ofSaudi journal of biological sciences · 2020
    Article
  10. Mechanisms protecting host cells against bacterial pore-forming toxins.Cellular and molecular life sciences : CMLS · 2019
    Review
  11. Article
  12. Article
  13. Review
  14. A Novel Role ofFrontiers in cellular and infection microbiology · 2017
    Article
  15. Article
  16. 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

1 author at 1 institution in 1 country.

Jacques MathieuDepartment of Microbiology, Institut de Recherche Biomédicale des Armées (IRBA), BP 73, Bretigny-sur-orge cedex F-91223, France. jacques.mathieu@irba.fr.
Institut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a physiological process involved in defense mechanisms for clearing intracellular bacteria. The autophagic pathway is finely regulated and bacterial toxins interact with this process in a complex manner. Bacterial toxins also interact significantly with many biochemical processes. Evaluations of the effects of bacterial toxins, such as endotoxins, pore-forming toxins and adenylate cyclases, on autophagy could support the development of new strategies for counteracting bacterial pathogenicity. Treatment strategies could focus on drugs that enhance autophagic processes to improve the clearance of intracellular bacteria. However, further in vivo studies are required to decipher the upregulation of autophagy and potential side effects limiting such approaches. The capacity of autophagy activation strategies to improve the outcome of antibiotic treatment should be investigated in the future.

Indexed as

AnimalsAnti-Bacterial AgentsAutophagyBacterial InfectionsBacterial ToxinsHumansAnti-Bacterial AgentsBacterial Toxinsautophagybacterial toxinscyclic AMPtherapeutic targets

Identifiers

PMID26248079
PMCPMC4549733
OpenAlexW1561736284

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.