Evidence map›Paper›PMID 31068826›Full record

ArticleFrontiers in physiology2019

The Mechanical Stimulation of Myotubes Counteracts the Effects of Tumor-Derived Factors Through the Modulation of the Activin/Follistatin Ratio.

Alexandra Baccam, Alexandra Benoni-Sviercovich, Marco Rocchi, Viviana Moresi, Marilia Seelaender, Zhenlin Li, Sergio Adamo, Zhigang Xue, Dario Coletti

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  17. A Pound of Flesh: What Cachexia Is and What It Is Not.Diagnostics (Basel, Switzerland) · 2021
    Review
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  20. Identification ofNutrients · 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

9 authors at 5 institutions in 3 countries.

Alexandra BaccamBiology of Adaptation and Aging (B2A), Sorbonne Université, UMR8256 - INSERM ERL U1164, Paris, France.
Alexandra Benoni-SviercovichBiology of Adaptation and Aging (B2A), Sorbonne Université, UMR8256 - INSERM ERL U1164, Paris, France.
Marco RocchiDepartment of Biomolecular Sciences, University of Urbino, Urbino, Italy.
Viviana MoresiSection of Histology, Department of Anatomical, Histological, Forensic and Orthopedic Sciences, Sapienza University of Rome, Rome, Italy.
Marilia SeelaenderInstitute of Biomedical Sciences, Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.
Zhenlin LiSection of Histology, Department of Anatomical, Histological, Forensic and Orthopedic Sciences, Sapienza University of Rome, Rome, Italy.
Sergio AdamoBiology of Adaptation and Aging (B2A), Sorbonne Université, UMR8256 - INSERM ERL U1164, Paris, France.
Zhigang XueSection of Histology, Department of Anatomical, Histological, Forensic and Orthopedic Sciences, Sapienza University of Rome, Rome, Italy.
Dario ColettiBiology of Adaptation and Aging (B2A), Sorbonne Université, UMR8256 - INSERM ERL U1164, Paris, France.
Adaptation Biologique et VieillissementSapienza University of Rome · ITInserm · FRUniversidade de São Paulo · BRUniversity of Urbino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activin negatively affects muscle fibers and progenitor cells in aging (sarcopenia) and in chronic diseases characterized by severe muscle wasting (cachexia). High circulating activin levels predict poor survival in cancer patients. However, the relative impact of activin in mediating muscle atrophy and hampered homeostasis is still unknown. To directly assess the involvement of activin, and its physiological inhibitor follistatin, in cancer-induced muscle atrophy, we cultured C2C12 myotubes in the absence or in the presence of a mechanical stretching stimulus and in the absence or presence of C26 tumor-derived factors (CM), so as to mimic the mechanical stimulation of exercise and cancer cachexia, respectively. We found that CM induces activin release by myotubes, further exacerbating the negative effects of tumor-derived factors. In addition, mechanical stimulation is sufficient to counteract the adverse tumor-induced effects on muscle cells, in association with an increased follistatin/activin ratio in the cell culture medium, indicating that myotubes actively release follistatin upon stretching. Recombinant follistatin counteracts tumor effects on myotubes exclusively by rescuing fusion index, suggesting that it is only partially responsible for the stretch-mediated rescue. Therefore, besides activin, other tumor-derived factors may play a significant role in mediating muscle atrophy. In addition to increasing follistatin secretion mechanical stimulation induces additional beneficial responses in myotubes. We propose that in animal models of cancer cachexia and in cancer patients purely mechanical stimuli play an important role in mediating the rescue of the muscle homeostasis reported upon exercise.

Indexed as

C26 colon carcinomaexerciseFlexCell apparatusmechanotransductionmyokinesskeletal muscle atrophy

Identifiers

PMID31068826
PMCPMC6491697
OpenAlexW2942123825

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Registered trials

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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.