Evidence map›Paper›PMID 25607549›Full record

ReviewDNA and cell biology2015

Autophagy in the fight against tuberculosis.

Carla F Bento, Nuno Empadinhas, Vítor Mendes

Abstract readReview
In one paragraph

Review in DNA and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. IFN-γ-Driven macrophage responses in the immunity toFrontiers in cellular and infection microbiology · 2025
    Review
  6. Review
  7. Estrogen and bacterial infection.Frontiers in immunology · 2025
    Review
  8. Review
  9. Journal of clinical tuberculosis and other mycobacterial diseases · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Exploring and exploiting the host cell autophagy during Mycobacterium tuberculosis infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2023
    Review
  16. Article
  17. The protective role ofFrontiers in medicine · 2023
    Article
  18. Article
  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.

Carla F Bento1 Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge , Cambridge, United Kingdom .
Nuno Empadinhas
Vítor Mendes

Funding

PHS HHS OPP1024021
6 · The paper itself

Abstract

Tuberculosis (TB), a chronic infectious disease mainly caused by the tubercle bacillus Mycobacterium tuberculosis, is one of the world's deadliest diseases that has afflicted humanity since ancient times. Although the number of people falling ill with TB each year is declining, its incidence in many developing countries is still a major cause of concern. Upon invading host cells by phagocytosis, M. tuberculosis can replicate within infected cells by arresting the maturation of the phagosome whose function is to target the pathogen for elimination. Host cells have mechanisms of controlling this evasion by inducing autophagy, an elaborate cellular process that targets bacteria for progressive elimination, decreasing bacterial loads within infected cells. In addition, autophagy activation also aids in the control of inflammation, contributing to a more efficient innate immune response against M. tuberculosis. Several innovative TB therapies have been envisaged based on autophagy manipulation, with some of them revealing high potential for future clinical trials and eventual implementation in healthcare systems. Thus, this review highlights the recent advances on the innate immune response regulation by autophagy upon M. tuberculosis infection and the promising new autophagy-based therapies for TB.

Indexed as

Drug DesignAnimalsAntitubercular AgentsAutophagyHumansImmunity, InnateMycobacterium tuberculosisTuberculosis, PulmonaryAntitubercular Agents

Identifiers

PMID25607549
PMCPMC4390021

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.