Evidence map›Paper›PMID 22172201›Full record

ReviewExpert reviews in molecular medicine2011

Redox homeostasis in mycobacteria: the key to tuberculosis control?

Ashwani Kumar, Aisha Farhana, Loni Guidry, Vikram Saini, Mary Hondalus, Adrie J C Steyn

Open access · bronzeAbstract readReview
In one paragraph

Review in Expert reviews in molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

112 citing papers in PubMed, 207 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Future Research Directions on Mycobacterium tuberculosis Proteins.Advances in experimental medicine and biology · 2026
    Review
  6. Article
  7. Article
  8. A Quinoxaline 1,4-Dioxide Activates DNA Repair Systems inInternational journal of molecular sciences · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Altered serine metabolism promotes drug tolerance inAntimicrobial agents and chemotherapy · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. The Benefits of Toxicity:Microorganisms · 2023
    Article
  19. Article
  20. Pathogens (Basel, Switzerland) · 2023
    Article

52 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Ashwani KumarInstitute of Microbial Technology, Chandigarh 160036, India.
Aisha Farhana
Loni Guidry
Vikram Saini
Mary Hondalus
Adrie J C Steyn
University of Alabama at Birmingham · USInstitute of Microbial Technology · INUniversity of Georgia · US

Funding

WhiB3 in M. tuberculosis virulenceR01AI058131 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STEYN, ADRIE JC · 2004 to 2014
$3.6M
Virulence of the opportunistic pathogen Rhodococcus equiR01AI060469 · NIAID · UNIVERSITY OF GEORGIA · PI HONDALUS, MARY · 2006 to 2010
$1.6M
MECHANISM OF MYCOBACTERIUM TUBERCULOSIS PERSISTENCER01AI076389 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STEYN, ADRIE JC · 2009 to 2012
$1.4M
Role of WhiB3 in M. tuberculosis virulenceR56AI058131 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STEYN, ADRIE JC · 2009 to 2009
$366k
NIAID NIH HHS AI058131NIAID NIH HHS AI060469NIAID NIH HHS AI076389NIAID NIH HHS R01 AI058131NIAID NIH HHS R01 AI060469NIAID NIH HHS R01 AI076389NIAID NIH HHS R56 AI058131
6 · The paper itself

Abstract

Mycobacterium tuberculosis (Mtb) is a metabolically flexible pathogen that has the extraordinary ability to sense and adapt to the continuously changing host environment experienced during decades of persistent infection. Mtb is continually exposed to endogenous reactive oxygen species (ROS) as part of normal aerobic respiration, as well as exogenous ROS and reactive nitrogen species (RNS) generated by the host immune system in response to infection. The magnitude of tuberculosis (TB) disease is further amplified by exposure to xenobiotics from the environment such as cigarette smoke and air pollution, causing disruption of the intracellular prooxidant-antioxidant balance. Both oxidative and reductive stresses induce redox cascades that alter Mtb signal transduction, DNA and RNA synthesis, protein synthesis and antimycobacterial drug resistance. As reviewed in this article, Mtb has evolved specific mechanisms to protect itself against endogenously produced oxidants, as well as defend against host and environmental oxidants and reductants found specifically within the microenvironments of the lung. Maintaining an appropriate redox balance is critical to the clinical outcome because several antimycobacterial prodrugs are only effective upon bioreductive activation. Proper homeostasis of oxido-reductive systems is essential for Mtb survival, persistence and subsequent reactivation. The progress and remaining deficiencies in understanding Mtb redox homeostasis are also discussed.

Indexed as

Bacterial ProteinsFree RadicalsHomeostasisHumansLungMycobacterium tuberculosisOxidation-ReductionOxidative StressTuberculosisBacterial ProteinsFree Radicals

Identifiers

PMID22172201
PMCPMC3241215
OpenAlexW2056874478

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.