Evidence map›Paper›PMID 27649272›Full record

ArticleJournal of cellular physiology2017

Heat Stress Modulates Both Anabolic and Catabolic Signaling Pathways Preventing Dexamethasone-Induced Muscle Atrophy In Vitro.

Wakako Tsuchida, Masahiro Iwata, Takayuki Akimoto, Shingo Matsuo, Yuji Asai, Shigeyuki Suzuki

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Article
  5. Potential Therapeutic Strategies for Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2022
    Review
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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

6 authors at 3 institutions in 1 country.

Wakako TsuchidaDepartment of Rehabilitation, Faculty of Health Sciences, Nihon Fukushi University, Handa, Aichi, Japan.
Masahiro IwataDepartment of Rehabilitation, Faculty of Health Sciences, Nihon Fukushi University, Handa, Aichi, Japan.
Takayuki AkimotoFaculty of Sport Sciences, Waseda University, Tokorozawa, Saitama, Japan.
Shingo MatsuoDepartment of Rehabilitation, Faculty of Health Sciences, Nihon Fukushi University, Handa, Aichi, Japan.
Yuji AsaiDepartment of Rehabilitation, Faculty of Health Sciences, Nihon Fukushi University, Handa, Aichi, Japan.
Shigeyuki SuzukiProgram in Physical and Occupational Therapy, Graduate School of Medicine, Nagoya University, Nagoya, Aichi, Japan.
Nagoya University · JPNihon Fukushi University · JPWaseda University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is generally recognized that synthetic glucocorticoids induce skeletal muscle weakness, and endogenous glucocorticoid levels increase in patients with muscle atrophy. It is reported that heat stress attenuates glucocorticoid-induced muscle atrophy; however, the mechanisms involved are unknown. Therefore, we examined the mechanisms underlying the effects of heat stress against glucocorticoid-induced muscle atrophy using C2C12 myotubes in vitro, focusing on expression of key molecules and signaling pathways involved in regulating protein synthesis and degradation. The synthetic glucocorticoid dexamethasone decreased myotube diameter and protein content, and heat stress prevented the morphological and biochemical glucocorticoid effects. Heat stress also attenuated increases in mRNAs of regulated in development and DNA damage responses 1 (REDD1) and Kruppel-like factor 15 (KLF15). Heat stress recovered the dexamethasone-induced inhibition of PI3K/Akt signaling. These data suggest that changes in anabolic and catabolic signals are involved in heat stress-induced protection against glucocorticoid-induced muscle atrophy. These results have a potentially broad clinical impact because elevated glucocorticoid levels are implicated in a wide range of diseases associated with muscle wasting. J. Cell. Physiol. 232: 650-664, 2017. © 2016 The Authors. Journal of Cellular Physiology published by Wiley Periodicals, Inc.

Indexed as

AnimalsCell LineDexamethasoneGene Expression RegulationGlycogen Synthase Kinase 3 betaHeat-Shock ResponseHSP72 Heat-Shock ProteinsMAP Kinase Signaling SystemMiceMuscle Fibers, SkeletalMuscle ProteinsMuscular AtrophyPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaDexamethasoneGlycogen Synthase Kinase 3 betaHSP72 Heat-Shock ProteinsMuscle ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaRNA, Messenger

Identifiers

PMID27649272
PMCPMC5132157
OpenAlexW2524762117

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.