Evidence map›Paper›PMID 28753922›Full record

ReviewJournal of clinical medicine2017

Evidence of Oxidative Stress and Secondary Mitochondrial Dysfunction in Metabolic and Non-Metabolic Disorders.

Karolina M Stepien, Robert Heaton, Scott Rankin, Alex Murphy, James Bentley, Darren Sexton, Iain P Hargreaves

Abstract 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 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing 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

83 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Blood phenylalanine lowering partially reverses white matter changes in a mouse model of phenylketonuria.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  14. Observational
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

23 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

7 authors.

Karolina M StepienThe Mark Holland Metabolic Unit Salford Royal NHS Foundation Trust Stott Lane, Salford M6 8HD, UK. kstepien@doctors.org.uk.
Robert HeatonSchool of Pharmacy, Liverpool John Moore University, Byrom Street, Liverpool L3 3AF, UK. r.heaton@2013.ljmu.ac.uk.
Scott RankinSchool of Pharmacy, Liverpool John Moore University, Byrom Street, Liverpool L3 3AF, UK. s.rankin@2014.ljmu.ac.uk.
Alex MurphySchool of Pharmacy, Liverpool John Moore University, Byrom Street, Liverpool L3 3AF, UK. a.murphy3@2013.ljmu.ac.uk.
James BentleySchool of Pharmacy, Liverpool John Moore University, Byrom Street, Liverpool L3 3AF, UK. j.bentley@2014.ljmu.ac.uk.
Darren SextonSchool of Pharmacy, Liverpool John Moore University, Byrom Street, Liverpool L3 3AF, UK. d.w.sexton@ljmu.ac.uk.
Iain P HargreavesSchool of Pharmacy, Liverpool John Moore University, Byrom Street, Liverpool L3 3AF, UK. i.p.hargreaves@ljmu.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction and oxidative stress have been implicated in the pathogenesis of a number of diseases and conditions. Oxidative stress occurs once the antioxidant defenses of the body become overwhelmed and are no longer able to detoxify reactive oxygen species (ROS). The ROS can then go unchallenged and are able to cause oxidative damage to cellular lipids, DNA and proteins, which will eventually result in cellular and organ dysfunction. Although not always the primary cause of disease, mitochondrial dysfunction as a secondary consequence disease of pathophysiology can result in increased ROS generation together with an impairment in cellular energy status. Mitochondrial dysfunction may result from either free radical-induced oxidative damage or direct impairment by the toxic metabolites which accumulate in certain metabolic diseases. In view of the importance of cellular antioxidant status, a number of therapeutic strategies have been employed in disorders associated with oxidative stress with a view to neutralising the ROS and reactive nitrogen species implicated in disease pathophysiology. Although successful in some cases, these adjunct therapies have yet to be incorporated into the clinical management of patients. The purpose of this review is to highlight the emerging evidence of oxidative stress, secondary mitochondrial dysfunction and antioxidant treatment efficacy in metabolic and non-metabolic diseases in which there is a current interest in these parameters.

Indexed as

catalasecoenzyme Q10electron transport chainglutathionemethylmalonic acidmethylmalonic acidemiamitochondrianitric oxide synthasenitrosative stressoxidative stressperoxisomephenylketonuriareactive nitrogen speciesreactive oxygen speciessepsissuperoxide dismutase

Identifiers

PMID28753922
PMCPMC5532579

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.