Evidence map›Paper›PMID 37740791›Full record

ReviewEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2023

Exploring and exploiting the host cell autophagy during Mycobacterium tuberculosis infection.

Pavan Kumar Nagdev, Puja Kumari Agnivesh, Arnab Roy, Shashikanta Sau, Nitin Pal Kalia

Abstract readReview
PubMed Publisher
In one paragraph

Review in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. TowardMicroorganisms · 2024
    Review
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

5 authors.

Pavan Kumar NagdevDepartment of Biological Sciences (Pharmacology and Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, Telangana, 500037, India.
Puja Kumari AgniveshDepartment of Biological Sciences (Pharmacology and Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, Telangana, 500037, India.
Arnab RoyDepartment of Biological Sciences (Pharmacology and Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, Telangana, 500037, India.
Shashikanta SauDepartment of Biological Sciences (Pharmacology and Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, Telangana, 500037, India.
Nitin Pal KaliaDepartment of Biological Sciences (Pharmacology and Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, Telangana, 500037, India. nitin.kalia@niperhyd.ac.in.ORCID http://orcid.org/0000-0003-4346-6567

Funding

Department of Biotechnology, Ministry of Science and Technology, India D.O.NO.BT/HRD/35/02/2006; NO. BT/RLF/Re-entry 66/2017; GAP-39
6 · The paper itself

Abstract

Tuberculosis, caused by Mycobacterium tuberculosis, is a fatal infectious disease that prevails to be the second leading cause of death from a single infectious agent despite the availability of multiple drugs for treatment. The current treatment regimen involves the combination of several drugs for 6 months that remain ineffective in completely eradicating the infection because of several drawbacks, such as the long duration of treatment and the side effects of drugs causing non-adherence of patients to the treatment regimen. Autophagy is an intracellular degradative process that eliminates pathogens at the early stages of infection. Mycobacterium tuberculosis's unique autophagy-blocking capability makes it challenging to eliminate compared to usual pathogens. The present review discusses recent advances in autophagy-inhibiting factors and mechanisms that could be exploited to identify autophagy-inducing chemotherapeutics that could be used as adjunctive therapy with the existing first-line anti-TB agent to shorten the duration of therapy and enhance cure rates from multidrug-resistant tuberculosis (MDR-TB) and extreme drug-resistant tuberculosis (XDR-TB).

Indexed as

AutophagyHost-Pathogen InteractionsMycobacterium tuberculosisTuberculosisAnimalsAntitubercular AgentsHumansTuberculosis, Multidrug-ResistantAntitubercular AgentsAutophagyHost cell inhibitorsHost defenseTuberculosis

Identifiers

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.