Evidence map›Paper›PMID 27215643›Full record

ReviewMammalian genome : official journal of the International Mammalian Genome Society2016

Ageing in relation to skeletal muscle dysfunction: redox homoeostasis to regulation of gene expression.

Katarzyna Goljanek-Whysall, Lesley A Iwanejko, Aphrodite Vasilaki, Vanja Pekovic-Vaughan, Brian McDonagh

Open access · hybridAbstract readReview
In one paragraph

Review in Mammalian genome : official journal of the International Mammalian Genome Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

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  9. Circadian regulation of muscle growth independent of locomotor activity.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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 1 institution in 1 country.

Katarzyna Goljanek-WhysallMRC-Arthritis Research UK Centre for Integrated research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8XL, UK. kwhysall@liverpool.ac.uk.
Lesley A IwanejkoMRC-Arthritis Research UK Centre for Integrated research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8XL, UK.
Aphrodite VasilakiMRC-Arthritis Research UK Centre for Integrated research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8XL, UK.
Vanja Pekovic-VaughanMRC-Arthritis Research UK Centre for Integrated research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8XL, UK.
Brian McDonaghMRC-Arthritis Research UK Centre for Integrated research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, L7 8XL, UK. bmcd@liverpool.ac.uk.
University of Liverpool · GB

Funding

Arthritis Research UKBiotechnology and Biological Sciences Research Council BB/L021668/1Medical Research Council MR/K006312/1Wellcome Trust 097826/Z/11/A
6 · The paper itself

Abstract

Ageing is associated with a progressive loss of skeletal muscle mass, quality and function-sarcopenia, associated with reduced independence and quality of life in older generations. A better understanding of the mechanisms, both genetic and epigenetic, underlying this process would help develop therapeutic interventions to prevent, slow down or reverse muscle wasting associated with ageing. Currently, exercise is the only known effective intervention to delay the progression of sarcopenia. The cellular responses that occur in muscle fibres following exercise provide valuable clues to the molecular mechanisms regulating muscle homoeostasis and potentially the progression of sarcopenia. Redox signalling, as a result of endogenous generation of ROS/RNS in response to muscle contractions, has been identified as a crucial regulator for the adaptive responses to exercise, highlighting the redox environment as a potentially core therapeutic approach to maintain muscle homoeostasis during ageing. Further novel and attractive candidates include the manipulation of microRNA expression. MicroRNAs are potent gene regulators involved in the control of healthy and disease-associated biological processes and their therapeutic potential has been researched in the context of various disorders, including ageing-associated muscle wasting. Finally, we discuss the impact of the circadian clock on the regulation of gene expression in skeletal muscle and whether disruption of the peripheral muscle clock affects sarcopenia and altered responses to exercise. Interventions that include modifying altered redox signalling with age and incorporating genetic mechanisms such as circadian- and microRNA-based gene regulation, may offer potential effective treatments against age-associated sarcopenia.

Indexed as

AgingCircadian ClocksGene Expression RegulationHomeostasisHumansMicroRNAsMuscle ContractionMuscle, SkeletalMuscular AtrophyOxidation-ReductionSarcopeniaMicroRNAs

Identifiers

PMID27215643
PMCPMC4935741
OpenAlexW2400686335

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.