Evidence map›Paper›PMID 30865638›Full record

ArticlePloS one2019

Pasakbumin A controls the growth of Mycobacterium tuberculosis by enhancing the autophagy and production of antibacterial mediators in mouse macrophages.

Hyo-Ji Lee, Hyun-Jeong Ko, Seung Hyun Kim, Yu-Jin Jung

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. MedComm · 2023
    Review
  7. Review
  8. Host-Directed Therapies for Tuberculosis.Pathogens (Basel, Switzerland) · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Rapamycin Promotes ROS-Mediated Cell DeathFrontiers in oncology · 2021
    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

4 authors at 2 institutions in 1 country.

Hyo-Ji LeeDepartment of Biological Sciences and Institute of Life Sciences, Kangwon National University, Chuncheon, Republic of Korea.
Hyun-Jeong KoCollege of Pharmacy, Kangwon National University, Chuncheon, Republic of Korea.
Seung Hyun KimCollege of Pharmacy, Yonsei University, Incheon, Republic of Korea.
Yu-Jin JungDepartment of Biological Sciences and Institute of Life Sciences, Kangwon National University, Chuncheon, Republic of Korea.ORCID 0000-0002-4942-677X
Kangwon National University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis (Mtb) and remains a major health problem worldwide. Thus, identification of new and more effective drugs to treat emerging multidrug-resistant TB (MDR-TB) and to reduce the side effects of anti-TB drugs, such as liver toxicity and other detrimental changes, is urgently needed. In this study, to develop a novel candidate drug for effective TB treatment with few side effects in the host, we selected pasakbumin A isolated from Eurycoma longifolia (E. longifolia) Jack, which protected host cells against Mtb infection-induced death. Pasakbumin A significantly inhibited intracellular Mtb growth by inducing the autophagy via the ERK1/2-mediated signaling pathway in Mtb-infected macrophages. We further investigated whether pasakbumin A could be used as a potential adjuvant for TB treatment. Treatment with pasakbumin A and anti-TB drug rifampicin (RMP) potently suppressed intracellular Mtb killing by promoting autophagy as well as TNF-α production via the ERK1/2- and NF-κB-mediated signaling pathways in Mtb-infected cells. Our results suggest that pasakbumin A could be developed as a novel anti-TB drug or host-directed therapeutic (HDT) strategy to protect against host cell death and improve host defense mechanisms against Mtb infection in macrophages.

Indexed as

AnimalsAntitubercular AgentsAutophagyDrug SynergismEurycomaHost-Pathogen InteractionsHumansInflammation MediatorsMacrophagesMAP Kinase Signaling SystemMiceMycobacterium tuberculosisNF-kappa BNitric OxidePlant ExtractsQuassinsAntitubercular AgentseurycomanoneInflammation MediatorsNF-kappa BNitric OxidePlant ExtractsQuassinsRifampinTumor Necrosis Factor-alpha

Identifiers

PMID30865638
PMCPMC6415846
OpenAlexW2952134384

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.