Evidence map›Paper›PMID 27382036›Full record

ReviewAmerican journal of physiology. Endocrinology and metabolism2016

Control of skeletal muscle atrophy in response to disuse: clinical/preclinical contentions and fallacies of evidence.

Philip J Atherton, Paul L Greenhaff, Stuart M Phillips, Sue C Bodine, Christopher M Adams, Charles H Lang

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05161975 (Effects of Vitamin K2 Supplements on Recovery of Lower Limb Muscle Function After Ankle Injury in Adults), which is not on this map. Cited by 91 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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.

NCT05161975 naunknown statusnot on this mapstarted 2021, after this paper: background citation

Effects of Vitamin K2 Supplements on Recovery of Lower Limb Muscle Function After Ankle Injury in Adults

TypeinterventionalSponsorLithuanian Sports UniversityRan2021 to 2023Enrolled60ConditionsMuscle Atrophy, CachexiaArmsVitamin K2
3 · Its place in the literature

Who cites it

91 citing papers in PubMed, 2 syntheses or guidelines pooled it, 159 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. Review
  10. Muscle atrophy after ACL reconstruction involves molecular mechanisms beyond unloading.Journal of applied physiology (Bethesda, Md. : 1985) · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. MuRF1 Partners With TRIM72 to Impair Insulin Signaling in Skeletal Muscle Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  18. Article
  19. Article
  20. Review

31 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

6 authors at 6 institutions in 3 countries.

Philip J AthertonRoyal Derby Medical School, Royal Derby Hospital, Derby, United Kingdom; Philip.atherton@nottingham.ac.uk.
Paul L GreenhaffMRC-ARUK Centre for Musculoskeletal Ageing Research, ARUK Centre for Sport, Exercise, and Osteoarthritis, School of Life Sciences, The Medical School, University of Nottingham, Nottingham, United Kingdom;
Stuart M PhillipsDepartment of Kinesiology, McMaster University, Hamilton, Ontario, Canada;
Sue C BodineDepartments of Neurobiology, Physiology and Behavior, and Physiology and Membrane Biology, University of California Davis, Veterans Affairs Northern California Health Care System, Mather, California;
Christopher M AdamsDepartments of Internal Mediciane and Molecular Physiology and Biophysics and Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, Iowa; Iowa City Veterans Affairs Medical Center, Iowa City, Iowa; and.
Charles H LangDepartment of Cellular and Molecular Physiology, Pennsylvania State College of Medicine, Hershey, Pennsylvania.
McMaster University · CAPenn State Milton S. Hershey Medical Center · USRoyal Derby Hospital · GBUniversity of Nottingham · GBVA Northern California Health Care System · USVeterans Health Administration · US

Funding

SEPSIS INDUCED INSULIN RESISTANCE IN DIABETESR01GM038032 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI LANG, CHARLES H. · 1992 to 2015
$5.4M
LAT1 and the development of anabolic resistanceR01AG045375 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BAAR, KEITH · 2014 to 2018
$1.7M
Molecular Pathogenesis of Skeletal Muscle AtrophyR01AR059115 · NIAMS · UNIVERSITY OF IOWA · PI ADAMS, CHRISTOPHER M · 2010 to 2014
$1.6M
Molecular Mechanisms of Age-related Muscle LossI01BX000976 · VA · IOWA CITY VA MEDICAL CENTER · PI YOREK, MARK A. · 2012 to 2022
–
Prevention and Treatment of Skeletal Muscle AtrophyI01RX001477 · VA · IOWA CITY VA MEDICAL CENTER · PI ADAMS, CHRISTOPHER M · 2015 to 2017
–
Biotechnology and Biological Sciences Research Council BB/G011435/1BLRD VA I01 BX000976Medical Research Council MR/K00414X/1NIAMS NIH HHS R01 AR059115NIA NIH HHS R01 AG045375NIGMS NIH HHS R01 GM038032RRD VA I01 RX001477
6 · The paper itself

Abstract

Muscle wasting resulting wholly or in part from disuse represents a serious medical complication that, when prolonged, can increase morbidity and mortality. Although much knowledge has been gained over the past half century, the underlying etiology by which disuse alters muscle proteostasis remains enigmatic. Multidisciplinary and novel methodologies are needed to fill gaps and overcome barriers to improved patient care. The present review highlights seminal concepts from a symposium at Experimental Biology 2016. These proceedings focus on 1) the role of insulin resistance in mediating disuse-induced changes in muscle protein synthesis (MPS) and breakdown (MPB), as well as cross-talk between carbohydrate and protein metabolism; 2) the relative importance of MPS/MPB in mediating involuntary muscle loss in humans and animals; 3) interpretative limitations associated with MPS/MPB "markers," e.g., MuRF1/MAFbx mRNA; and finally, 4) how OMIC technologies can be leveraged to identify molecular pathways (e.g., ATF4, p53, p21) mediating disuse atrophy. This perspective deals primarily with "simple atrophy" due to unloading. Nonetheless, it is likely that disuse is a pervasive contributor to muscle wasting associated with catabolic disease-related atrophy (i.e., due to associated sedentary behaviour of disease burden). Key knowledge gaps and challenges are identified to stimulate discussion and identify opportunities for translational research. Data from animal and human studies highlight both similarities and differences. Integrated preclinical and clinical research is encouraged to better understand the metabolic and molecular underpinnings and translational relevance,for disuse atrophy. These approaches are crucial to clinically prevent or reverse muscle atrophy, thereby reestablishing homeostasis and recovery.

Indexed as

AnimalsHumansMuscle ProteinsMuscle, SkeletalMuscular AtrophyMuscular Disorders, AtrophicProtein BiosynthesisMuscle Proteinsactivating transcription factor 4disuse atrophymuscle ring finger 1protein degradationprotein synthesis

Identifiers

PMID27382036
PMCPMC5142005
OpenAlexW2462542303

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.