Mycobacterium tuberculosis: prePPARing and Maintaining the Replicative Niche.

Michael D Stutz, Marc Pellegrini

Abstract readComment

In one paragraph

Article in Trends in microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it

0cells of the map it votes in

3citing papers in PubMed

0.1field-weighted citation impact, top 50% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

PPE57 Cooperates with MmpL3 to Mediate Bacterial Lipid Transport and Promote Persistent Infection ofMicroorganisms · 2026
Article
Activation of transcription factor CREB in human macrophages by Mycobacterium tuberculosis promotes bacterial survival, reduces NF-kB nuclear transit and limits phagolysosome fusion by reduced necroptotic signaling.PLoS pathogens · 2023
Article
Infiltration of Apoptotic M2 Macrophage Subpopulation Is Negatively Correlated with the Immunotherapy Response in Colorectal Cancer.International journal of molecular sciences · 2022
Article

4 · The record

Corrections and comments

Comment on
PPARγ is critical for Mycobacterium tuberculosis induction of Mcl-1 and limitation of human macrophage apoptosis.2018

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Michael D StutzInfection and Immunity Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; Department of Medical Biology, The University of Melbourne, Melbourne, VIC, Australia.

Marc PellegriniInfection and Immunity Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; Department of Medical Biology, The University of Melbourne, Melbourne, VIC, Australia. Electronic address: pellegrini@wehi.edu.au.

University of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium tuberculosis interferes with the ability of its host cell to undergo apoptosis. Arnett et al. report that the pathogen promotes macrophage survival by engaging the nuclear receptor PPARγ to induce the antiapoptotic protein MCL-1, yielding insights into the pathogenesis of tuberculosis and potentially unlocking new avenues for therapeutic intervention.

Indexed as

Mycobacterium tuberculosisTuberculosisApoptosisHumansMacrophagesMyeloid Cell Leukemia Sequence 1 ProteinPPAR gammaMyeloid Cell Leukemia Sequence 1 ProteinPPAR gammaapoptosishost-directed therapyMCL-1PPARγtuberculosis

Identifiers

PMID30119946

DOI10.1016/j.tim.2018.08.001

OpenAlexW2887357086

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.