Evidence map›Paper›PMID 29239106›Full record

ReviewThe FEBS journal2019

ER stress in skeletal muscle remodeling and myopathies.

Dil Afroze, Ashok Kumar

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in The FEBS journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06660784 (Mechanism of Nitric Oxide on Ventilator-induced Diaphragm Dysfunction with Extracorporeal Membrane Lung Assistance), which is not on this map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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.

NCT06660784 active not recruitingnot on this mapstarted 2024, after this paper: background citation

Mechanism of Nitric Oxide on Ventilator-induced Diaphragm Dysfunction with Extracorporeal Membrane Lung Assistance

TypeobservationalSponsorZhongnan HospitalRan2024 to 2025Enrolled80ConditionsTracheal Intubation, Extracorporeal Membrane Oxygenation, Nitric Oxide, Ventilator-induced Diaphragmatic DysfunctionArmsNitric Oxide
3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. TAK1 Regulates Skeletal Muscle Mass, Hypertrophic Signaling, and Metabolic Homeostasis in Male and Female Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. The Role of C/EBP-Homologous Protein in Idiopathic Inflammatory Myopathies.Journal of cellular and molecular medicine · 2025
    Article
  18. Review
  19. The multimodal transcriptional response of denervated skeletal muscle involves regulation ofProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Review

36 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

2 authors at 1 institution in 2 countries.

Dil AfrozeDepartment of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, KY, USA.
Ashok KumarDepartment of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, KY, USA.
University of Louisville · US

Funding

TAK1/TRAF6 Signaling in Skeletal MuscleR01AR059810 · NIAMS · UNIVERSITY OF LOUISVILLE · PI KUMAR, ASHOK · 2011 to 2021
$4.0M
Role of TWEAK in Skeletal Muscle MetabolismR01AG029623 · NIA · UNIVERSITY OF LOUISVILLE · PI KUMAR, ASHOK · 2007 to 2016
$2.8M
MYD88 Signaling in Mammalian Myoblast FusionR01AR068313 · NIAMS · UNIVERSITY OF LOUISVILLE · PI KUMAR, ASHOK · 2015 to 2019
$1.7M
NIAMS NIH HHS R01 AR059810NIAMS NIH HHS R01 AR068313NIA NIH HHS R01 AG029623
6 · The paper itself

Abstract

Skeletal muscle is a highly plastic tissue in the human body that undergoes extensive adaptation in response to environmental cues, such as physical activity, metabolic perturbation, and disease conditions. The endoplasmic reticulum (ER) plays a pivotal role in protein folding and calcium homeostasis in many mammalian cell types, including skeletal muscle. However, overload of misfolded or unfolded proteins in the ER lumen cause stress, which results in the activation of a signaling network called the unfolded protein response (UPR). The UPR is initiated by three ER transmembrane sensors: protein kinase R-like endoplasmic reticulum kinase, inositol-requiring protein 1α, and activating transcription factor 6. The UPR restores ER homeostasis through modulating the rate of protein synthesis and augmenting the gene expression of many ER chaperones and regulatory proteins. However, chronic heightened ER stress can also lead to many pathological consequences including cell death. Accumulating evidence suggests that ER stress-induced UPR pathways play pivotal roles in the regulation of skeletal muscle mass and metabolic function in multiple conditions. They have also been found to be activated in skeletal muscle under catabolic states, degenerative muscle disorders, and various types of myopathies. In this article, we have discussed the recent advancements toward understanding the role and mechanisms through which ER stress and individual arms of the UPR regulate skeletal muscle physiology and pathology.

Indexed as

Endoplasmic Reticulum StressUnfolded Protein ResponseAnimalsEndoplasmic ReticulumHumansMuscle, SkeletalMuscular DiseasesProtein FoldingSignal TransductionER stressmetabolismmyogenesismyopathiesskeletal muscle atrophyunfolded protein response

Identifiers

PMID29239106
PMCPMC6002870
OpenAlexW2774342749

What OpenQuestion holds

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Registered trials

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.