Evidence map›Paper›PMID 23412895›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2013

Molecular mechanisms underlying skeletal muscle weakness in human cancer: reduced myosin-actin cross-bridge formation and kinetics.

Michael J Toth, Mark S Miller, Damien M Callahan, Andrew P Sweeny, Ivette Nunez, Steven M Grunberg, Hirak Der-Torossian, Marion E Couch, Kim Dittus

Open access · greenAbstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 56 citations in OpenAlex.

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  15. Influenza Infection has Fiber Type-Specific Effects on Cellular and Molecular Skeletal Muscle Function in Aged Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020
    Article
  16. Effects of an exercise-based oncology rehabilitation program and age on strength and physical function in cancer survivors.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2020
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  19. Maintenance of skeletal muscle function following reduced daily physical activity in healthy older adults: a pilot trial.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2019
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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

9 authors at 1 institution in 1 country.

Michael J TothDepartment of Medicine, University of Vermont, College of Medicine, Burlington, VT, USA. michael.toth@uvm.edu
Mark S Miller
Damien M Callahan
Andrew P Sweeny
Ivette Nunez
Steven M Grunberg
Hirak Der-Torossian
Marion E Couch
Kim Dittus
University of Vermont · US

Funding

POST-DOCTORAL CARDIOVASCULAR RESEARCH TRAINING PROGRAMT32HL007647 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI LEWINTER, MARTIN M · 1988 to 2013
$3.3M
Single Skeletal Muscle Fiber Mechanics and Myosin Kinetics in Human AgingK01AG031303 · NIA · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI MILLER, MARK STUART · 2008 to 2012
$611k
NHLBI NIH HHS HL-007647NHLBI NIH HHS T32 HL007647NIA NIH HHS AG-031303NIA NIH HHS K01 AG031303
6 · The paper itself

Abstract

Many patients with cancer experience physical disability following diagnosis, although little is known about the mechanisms underlying these functional deficits. To characterize skeletal muscle adaptations to cancer in humans, we evaluated skeletal muscle structure and contractile function at the molecular, cellular, whole-muscle, and whole-body level in 11 patients with cancer (5 cachectic, 6 noncachectic) and 6 controls without disease. Patients with cancer showed a 25% reduction in knee extensor isometric torque after adjustment for muscle mass (P < 0.05), which was strongly related to diminished power output during a walking endurance test (r = 0.889; P < 0.01). At the cellular level, single fiber isometric tension was reduced in myosin heavy chain (MHC) IIA fibers (P = 0.05) in patients with cancer, which was explained by a reduction (P < 0.05) in the number of strongly bound cross-bridges. In MHC I fibers, myosin-actin cross-bridge kinetics were reduced in patients, as evidenced by an increase in myosin attachment time (P < 0.01); and reductions in another kinetic parameter, myosin rate of force production, predicted reduced knee extensor isometric torque (r = 0.689; P < 0.05). Patients with cancer also exhibited reduced mitochondrial density (-50%; P < 0.001), which was related to increased myosin attachment time in MHC I fibers (r = -0.754; P < 0.01). Finally, no group differences in myofilament protein content or ultrastructure were noted that explained the observed functional alterations. Collectively, our results suggest reductions in myofilament protein function as a potential molecular mechanism contributing to muscle weakness and physical disability in human cancer.

Indexed as

ActinsAgedFemaleHumansIsometric ContractionKineticsMaleMiddle AgedMuscle, SkeletalMuscle WeaknessMyosin Heavy ChainsNeoplasmsActinsMyosin Heavy Chains

Identifiers

PMID23412895
PMCPMC3633441
OpenAlexW2024372043

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.