Evidence map›Paper›PMID 16002444›Full record

ReviewThe Journal of physiology2005

Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: role of ionic changes.

D G Allen, N P Whitehead, E W Yeung

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
4.8field-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

77 citing papers in PubMed, 195 citations in OpenAlex.

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  12. Differences in lumbar paraspinal muscle morphology in patients with sagittal malalignment undergoing posterior lumbar fusion surgery.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2022
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17 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

3 authors at 2 institutions in 2 countries.

D G AllenSchool of Medical Sciences, University of Sydney, NSW, Australia. davida@physiol.usyd.edu.au
N P Whitehead
E W Yeung
University of Sydney · AUHong Kong Polytechnic University · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle damage, characterized by prolonged weakness and delayed onset of stiffness and soreness, is common following contractions in which the muscles are stretched. Stretch-induced damage of this sort is more pronounced in the muscular dystrophies and the profound muscle damage observed in these conditions may involve similar pathways. It has been known for many years that damaged muscles accumulate calcium and that elevating calcium in normal muscles simulates many aspects of muscle damage. The changes in intracellular calcium, sodium and pH following stretched contractions are reviewed and the various pathways which have been proposed to allow ion entry are discussed. One possibility is that TRPC1 (transient receptor potential, canonical), a protein which seems to form both a stretch-activated channel and a store-operated channel, is the main source of Ca(2+) entry. The mechanisms by which the changes in intracellular ions contribute to reduced force production, to increased protein breakdown and to increased membrane permeability are considered. A hypothetical scheme for muscle damage which incorporates these ideas is presented.

Indexed as

Muscle ContractionAnimalsCalciumHumansHydrogen-Ion ConcentrationMuscle, SkeletalMuscular DiseasesMuscular DystrophiesSodiumTRPC Cation ChannelsCalciumSodiumtransient receptor potential cation channel, subfamily C, member 1TRPC Cation Channels

Identifiers

PMID16002444
PMCPMC1474216
OpenAlexW2162646067

What OpenQuestion holds

Textmetadata
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.