Evidence map›Paper›PMID 21807613›Full record

ArticleThe Journal of physiology2011

Muscle sparing in muscle RING finger 1 null mice: response to synthetic glucocorticoids.

Leslie M Baehr, J David Furlow, Sue C Bodine

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
8.4field-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.

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

127 citing papers in PubMed, 227 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Effect of NF-κB on Myosin Heavy Chain Content and Muscle Atrophy After Laryngeal Muscle Denervation.World journal of otorhinolaryngology - head and neck surgery · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. 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
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Autoimmune blistering diseases treated with glucocorticoids: An international study of steroid-induced myopathy.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025
    Article
  17. Article
  18. Muscle Disuse Atrophy.Advances in experimental medicine and biology · 2025
    Review
  19. Article
  20. Targeting MuRF1 to Combat Skeletal Muscle Wasting in Cardiac Cachexia: Mechanisms and Therapeutic Prospects.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Review

67 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Leslie M BaehrDepartment of Neurobiology, Physiology, and Behavior, University of California-Davis, One Shields Avenue, Davis, CA 95616, USA.
J David Furlow
Sue C Bodine
Laboratoire de Biologie Physico-Chimique des Protéines Membranaires · FRUniversity of California, Davis · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI PRIMO N. LARA · 2002 to 2026
$84.9M
Glucocorticoid control of gene expression during skeletal muscle atrophyR01DK075801 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BODINE, SUE C, FURLOW, JOHN DAVID · 2008 to 2011
$1.4M
NCI NIH HHS P30 CA093373NIDDK NIH HHS DK75801NIDDK NIH HHS R01 DK075801
6 · The paper itself

Abstract

Skeletal muscle atrophy occurs under a variety of conditions and can result from alterations in both protein synthesis and protein degradation. The muscle-specific E3 ubiquitin ligases, MuRF1 and MAFbx, are excellent markers of muscle atrophy and increase under divergent atrophy-inducing conditions such as denervation and glucocorticoid treatment. While deletion of MuRF1 or MAFbx has been reported to spare muscle mass following 14 days of denervation, their role in other atrophy-inducing conditions is unclear. The goal of this study was to determine whether deletion of MuRF1 or MAFbx attenuates muscle atrophy after 2 weeks of treatment with the synthetic glucocorticoid dexamethasone (DEX). The response of the triceps surae (TS) and tibialis anterior (TA) muscles to 14 days of DEX treatment (3 mg kg(-1) day(-1)) was examined in 4 month-old male and female wild type (WT) and MuRF1 or MAFbx knock out (KO) mice. Following 14 days of DEX treatment, muscle wet weight was significantly decreased in the TS and TA of WT mice. Comparison of WT and KO mice following DEX treatment revealed significant sparing of mass in both sexes of the MuRF1 KO mice, but no muscle sparing in MAFbx KO mice. Further analysis of the MuRF1 KO mice showed significant sparing of fibre cross-sectional area and tension output in the gastrocnemius (GA) after DEX treatment. Muscle sparing in the MuRF1 KO mice was related to maintenance of protein synthesis, with no observed increases in protein degradation in either WT or MuRF1 KO mice. These results demonstrate that MuRF1 and MAFbx do not function similarly under all atrophy models, and that the primary role of MuRF1 may extend beyond controlling protein degradation via the ubiquitin proteasome system.

Indexed as

AnimalsDexamethasoneFemaleForkhead Transcription FactorsGlucocorticoidsMaleMiceMice, Inbred C57BLMice, KnockoutMuscle ContractionMuscle ProteinsMuscle, SkeletalMuscular AtrophyProteasome Endopeptidase ComplexProtein BiosynthesisProteolysisDexamethasoneFbxo32 protein, mouseForkhead Transcription FactorsGlucocorticoidsMuscle ProteinsProteasome Endopeptidase ComplexSKP Cullin F-Box Protein LigasesTrim63 protein, mouseTripartite Motif ProteinsUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID21807613
PMCPMC3213422
OpenAlexW1590930560

What OpenQuestion holds

Textmetadata
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.