Evidence map›Paper›PMID 32644910›Full record

ReviewJournal of applied physiology (Bethesda, Md. : 1985)2020

Edward F. Adolph Distinguished Lecture. Skeletal muscle atrophy: Multiple pathways leading to a common outcome.

Sue C Bodine

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of applied physiology (Bethesda, Md. : 1985), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

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  19. Beta-hydroxy-beta-methylbutyrate associated with low-intensity exercise training improves skeletal muscle regeneration through the IGF-Akt pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022
    Article
  20. Exercise as a Peripheral Circadian Clock Resynchronizer in Vascular and Skeletal Muscle Aging.International journal of environmental research and public health · 2021
    Review
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

1 author at 1 institution in 1 country.

Sue C BodineDepartment of Internal Medicine/Endocrinology and Metabolism, University of Iowa Carver College of Medicine, Iowa City, Iowa.
University of Iowa · US

Funding

The Role of Intramuscular Lipids in Muscle Anabolic ResistanceR01AR070031 · NIAMS · UNIVERSITY OF IOWA · PI BODINE, SUE C, RUTLEDGE, JOHN CALVERT · 2016 to 2020
$2.3M
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
NIAID NIH HHS AR070031NIAMS NIH HHS R01 AR070031NIDDK NIH HHS DK075801NIDDK NIH HHS R01 DK075801RRD VA I01 RX000673VA 1I0RX000673
6 · The paper itself

Abstract

Skeletal muscle atrophy continues to be a serious consequence of many diseases and conditions for which there is no treatment. Our understanding of the mechanisms regulating skeletal muscle mass has improved considerably over the past two decades. For many years it was known that skeletal muscle atrophy resulted from an imbalance between protein synthesis and protein breakdown, with the net balance shifting toward protein breakdown. However, the molecular and cellular mechanisms underlying the increased breakdown of myofibrils was unknown. Over the past two decades, numerous reports have identified novel genes and signaling pathways that are upregulated and activated in response to stimuli such as disuse, inflammation, metabolic stress, starvation and others that induce muscle atrophy. This review summarizes the discovery efforts performed in the identification of several pathways involved in the regulation of skeletal muscle mass: the mammalian target of rapamycin (mTORC1) and the ubiquitin proteasome pathway and the E3 ligases, MuRF1 and MAFbx. While muscle atrophy is a common outcome of many diseases, it is doubtful that a single gene or pathway initiates or mediates the breakdown of myofibrils. Interestingly, however, is the observation that upregulation of the E3 ligases, MuRF1 and MAFbx, is a common feature of many divergent atrophy conditions. The challenge for the field of muscle biology is to understand how all of the various molecules, transcription factors, and signaling pathways interact to produce muscle atrophy and to identify the critical factors for intervention.

Indexed as

Muscular AtrophyUbiquitin-Protein LigasesHumansMuscle, SkeletalProtein BiosynthesisSignal TransductionSKP Cullin F-Box Protein LigasesTranscription FactorsTripartite Motif ProteinsSKP Cullin F-Box Protein LigasesTranscription FactorsTripartite Motif ProteinsUbiquitin-Protein LigasesMAFbxmTORC1MuRF1protein synthesisubiquitin proteasome pathway

Identifiers

PMID32644910
PMCPMC7473948
OpenAlexW3041828127

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.