Evidence map›Paper›PMID 29077060›Full record

ReviewJournal of clinical medicine2017

Oxidative Stress: Mechanistic Insights into Inherited Mitochondrial Disorders and Parkinson's Disease.

Mesfer Al Shahrani, Simon Heales, Iain Hargreaves, Michael Orford

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 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Mosses in Urban Environments as Passive Biofilters and Organisms Impacted by Asbestos-Contaminated Habitats.International journal of environmental research and public health · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. A pilot study of mitochondrial response to an in vivo prosthetic joint Staphylococcus aureus infection model.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Coenzyme Q10, Ageing and the Nervous System: An Overview.Antioxidants (Basel, Switzerland) · 2021
    Review
  19. Review
  20. Natural Compounds Attenuate Denervation-Induced Skeletal Muscle Atrophy.International journal of molecular sciences · 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

4 authors.

Mesfer Al ShahraniNeurometabolic Unit. National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. mesfer.shahrani.14@ucl.ac.uk.
Simon HealesNeurometabolic Unit. National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. s.heales@ucl.ac.uk.
Iain HargreavesNeurometabolic Unit. National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. i.p.hargreaves@ljmu.ac.uk.
Michael OrfordDepartment of Genetics and Genomic Medicine, UCL Great Ormond Street Institute of Child Health, London WC1N 1EH, UK. m.orford@ucl.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress arises when cellular antioxidant defences become overwhelmed by a surplus generation of reactive oxygen species (ROS). Once this occurs, many cellular biomolecules such as DNA, lipids, and proteins become susceptible to free radical-induced oxidative damage, and this may consequently lead to cellular and ultimately tissue and organ dysfunction. Mitochondria, as well as being a source of ROS, are vulnerable to oxidative stress-induced damage with a number of key biomolecules being the target of oxidative damage by free radicals, including membrane phospholipids, respiratory chain complexes, proteins, and mitochondrial DNA (mt DNA). As a result, a deficit in cellular energy status may occur along with increased electron leakage and partial reduction of oxygen. This in turn may lead to a further increase in ROS production. Oxidative damage to certain mitochondrial biomolecules has been associated with, and implicated in the pathophysiology of a number of diseases. It is the purpose of this review to discuss the impact of such oxidative stress and subsequent damage by reviewing our current knowledge of the pathophysiology of several inherited mitochondrial disorders together with our understanding of perturbations observed in the more commonly acquired neurodegenerative disorders such as Parkinson's disease (PD). Furthermore, the potential use and feasibility of antioxidant therapies as an adjunct to lower the accumulation of damaging oxidative species and hence slow disease progression will also be discussed.

Indexed as

antioxidantmitochondriaoxidative stressreactive oxygen species

Identifiers

PMID29077060
PMCPMC5704117

What OpenQuestion holds

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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.