Evidence map›Paper›PMID 30300394›Full record

ArticlePloS one2018

Muscle regeneration is disrupted by cancer cachexia without loss of muscle stem cell potential.

Shoya Inaba, Atsushi Hinohara, Masashi Tachibana, Kazutake Tsujikawa, So-Ichiro Fukada

Abstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  14. Article
  15. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
  16. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
  17. Review
  18. Article
  19. Cancer cachexia as a multiorgan failure: Reconstruction of the crime scene.Frontiers in cell and developmental biology · 2022
    Review
  20. Article
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.

Shoya InabaLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, Japan.
Atsushi HinoharaImmunology & Allergy Research Laboratories, Immunology & Allergy R&D Unit, R&D Division, Kyowa Hakko Kirin Co., Ltd., Nagaizumi-cho, Sunto-gun, Shizuoka, Japan.
Masashi TachibanaProject for Vaccine and Immune Regulation, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, Japan.ORCID 0000-0002-0376-508X
Kazutake TsujikawaLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, Japan.
So-Ichiro FukadaProject for Muscle Stem Cell Biology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, Japan.ORCID 0000-0003-4051-5108

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cachexia is a severe, debilitating condition characterized by progressive body wasting associated with remarkable loss of skeletal muscle weight. It has been reported that cancer cachexia disturbs the regenerative ability of skeletal muscle, but the cellular mechanisms are still unknown. Here, we investigated the skeletal muscle regenerative process in mouse colon-26 (C26) tumor cell-bearing mice as a C26 cancer cachexia model. Although the proliferation and differentiation abilities of muscle stem cells derived from the C26 tumor cell-bearing mice were sustained in vitro, the proliferation and differentiation were severely impaired in the cachexic mice. The numbers of both macrophages and mesenchymal progenitors, which are critical players in muscle regeneration, were reduced in the cancer cachexic mice, indicating that the skeletal muscle regeneration process was disrupted by cancer cachexia. Furthermore, the number of infiltrated neutrophils was also reduced in cancer cachexia mice 24 hours after muscle injury, and the expression of critical chemokines for muscle regeneration was reduced in cancer cachexia model mice compared to control mice. Collectively, although the ability to regeneration of MuSCs was retained, cancer cachexia disturbed skeletal muscle regenerative ability by inhibiting the orchestrated muscle regeneration processes.

Indexed as

RegenerationAdipose TissueAnimalsCachexiaCell DifferentiationCell Line, TumorCell ProliferationChemokinesCobra Cardiotoxin ProteinsColonic NeoplasmsCrotoxinDisease Models, AnimalDown-RegulationDrug CombinationsMiceMuscle, Skeletalcardiotoxin, crotoxin drug combinationChemokinesCobra Cardiotoxin ProteinsCrotoxinDrug Combinations

Identifiers

PMID30300394
PMCPMC6177180

What OpenQuestion holds

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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.