Evidence map›Paper›PMID 28744984›Full record

ReviewJournal of cachexia, sarcopenia and muscle2017

Redox homeostasis and age-related deficits in neuromuscular integrity and function.

Giorgos K Sakellariou, Adam P Lightfoot, Kate E Earl, Martin Stofanko, Brian McDonagh

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cachexia, sarcopenia and muscle, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Lipotoxicity-related sarcopenia: a review.Journal of medicine and life · 2022
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Exercise-induced oxidative stress: Friend or foe?Journal of sport and health science · 2020
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 4 institutions in 2 countries.

Giorgos K SakellariouGeneFirst Ltd, Culham Science Centre, Abingdon, Oxfordshire, OX14 3DB, UK.
Adam P LightfootSchool of Healthcare Science, Manchester Metropolitan University, Manchester, M1 5GD, UK.
Kate E EarlMRC-Arthritis Research UK Centre for Integrated Research into Musculoskeletal Ageing, Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Martin StofankoMicrovisk Technologies Ltd, The Quorum, 7600 Oxford Business Park, Oxford, OX4 2JZ, UK.
Brian McDonaghMRC-Arthritis Research UK Centre for Integrated Research into Musculoskeletal Ageing, Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8TX, UK.
Versus Arthritis · GBCulham Science Centre · GBManchester Metropolitan University · GBOxford Technologies (United Kingdom) · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Skeletal muscle is a major site of metabolic activity and is the most abundant tissue in the human body. Age-related muscle atrophy (sarcopenia) and weakness, characterized by progressive loss of lean muscle mass and function, is a major contributor to morbidity and has a profound effect on the quality of life of older people. With a continuously growing older population (estimated 2 billion of people aged >60 by 2050), demand for medical and social care due to functional deficits, associated with neuromuscular ageing, will inevitably increase. Despite the importance of this 'epidemic' problem, the primary biochemical and molecular mechanisms underlying age-related deficits in neuromuscular integrity and function have not been fully determined. Skeletal muscle generates reactive oxygen and nitrogen species (RONS) from a variety of subcellular sources, and age-associated oxidative damage has been suggested to be a major factor contributing to the initiation and progression of muscle atrophy inherent with ageing. RONS can modulate a variety of intracellular signal transduction processes, and disruption of these events over time due to altered redox control has been proposed as an underlying mechanism of ageing. The role of oxidants in ageing has been extensively examined in different model organisms that have undergone genetic manipulations with inconsistent findings. Transgenic and knockout rodent studies have provided insight into the function of RONS regulatory systems in neuromuscular ageing. This review summarizes almost 30 years of research in the field of redox homeostasis and muscle ageing, providing a detailed discussion of the experimental approaches that have been undertaken in murine models to examine the role of redox regulation in age-related muscle atrophy and weakness.

Indexed as

HomeostasisOxidation-ReductionAge FactorsAgingAnimalsAnimals, Genetically ModifiedAntioxidantsGene Expression Regulation, EnzymologicHumansMitochondriaModels, AnimalMotor NeuronsMuscle, SkeletalNeuromuscular JunctionOrgan SizeReactive Nitrogen SpeciesAntioxidantsReactive Nitrogen SpeciesReactive Oxygen SpeciesFrailtyMitochondriaMotor neuronsNeuromuscular junctionRedox signallingSuperoxide dismutase

Identifiers

PMID28744984
PMCPMC5700439
OpenAlexW2738955684

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.