Evidence map›Paper›PMID 28467362›Full record

ReviewJournal of clinical medicine2017

Glutathione as a Redox Biomarker in Mitochondrial Disease-Implications for Therapy.

Gregory M Enns, Tina M Cowan

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.6field-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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Therapies for Mitochondrial Disease: Past, Present, and Future.Journal of inherited metabolic disease · 2025
    Review
  4. Review
  5. Anti-aging activities of an ethanolic extract ofFrontiers in pharmacology · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. The Biochemical Assessment of Mitochondrial Respiratory Chain Disorders.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Extending the Scope ofAnalytical chemistry · 2021
    Article
  18. Article
  19. Review
  20. Coenzyme QAntioxidants (Basel, Switzerland) · 2021
    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

2 authors at 1 institution in 1 country.

Gregory M EnnsDepartments of Pediatrics and Pathology, Stanford University, 300 Pasteur Drive, H-315, Stanford, CA 94005-5208, USA. greg.enns@stanford.edu.
Tina M CowanDepartments of Pediatrics and Pathology, Stanford University, 300 Pasteur Drive, H-315, Stanford, CA 94005-5208, USA. tina.cowan@stanford.edu.
Stanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Technical advances in the ability to measure mitochondrial dysfunction are providing new insights into mitochondrial disease pathogenesis, along with new tools to objectively evaluate the clinical status of mitochondrial disease patients. Glutathione (l-ϒ-glutamyl-l-cysteinylglycine) is the most abundant intracellular thiol, and the intracellular redox state, as reflected by levels of oxidized (GSSG) and reduced (GSH) glutathione, as well as the GSH/GSSG ratio, is considered to be an important indication of cellular health. The ability to quantify mitochondrial dysfunction in an affected patient will not only help with routine care, but also improve rational clinical trial design aimed at developing new therapies. Indeed, because multiple disorders have been associated with either primary or secondary deficiency of the mitochondrial electron transport chain and redox imbalance, developing mitochondrial therapies that have the potential to improve the intracellular glutathione status has been a focus of several clinical trials over the past few years. This review will also discuss potential therapies to increase intracellular glutathione with a focus on EPI-743 (α-tocotrienol quinone), a compound that appears to have the ability to modulate the activity of oxidoreductases, in particular NAD(P)H:quinone oxidoreductase 1.

Indexed as

cysteamineEPI-743glutathionemitochondrial diseaseN-acetylcysteineredox imbalanceRP103

Identifiers

PMID28467362
PMCPMC5447941
OpenAlexW2610514232

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.