Evidence map›Paper›PMID 23872437›Full record

ReviewThe international journal of biochemistry & cell biology2013

Muscle wasting from kidney failure-a model for catabolic conditions.

Xiaonan H Wang, William E Mitch

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The international journal of biochemistry & cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 80 citations in OpenAlex.

  1. Effect of Long-term Exercise Training on Physical Performance and Cardiorespiratory Function in Adults With CKD: A Randomized Controlled Trial.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2023
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  9. Osteosarcopenia in Chronic Kidney Disease: An Overlooked Syndrome?Journal of cachexia, sarcopenia and muscle · 2025
    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

2 authors at 2 institutions in 1 country.

Xiaonan H WangRenal Division, Department of Medicine, Emory University, Atlanta, GA 30322, USA. xwang03@emory.edu
William E Mitch
Baylor College of Medicine · USEmory University · US

Funding

PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR37DK037175 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2006 to 2015
$3.8M
MicroRNA and Muscle Wasting in UremiaR01AR060268 · NIAMS · EMORY UNIVERSITY · PI WANG, XIAONAN H · 2012 to 2016
$1.7M
NIAMS NIH HHS R01 AR060268NIDDK NIH HHS R37 DK037175
6 · The paper itself

Abstract

purposeMuscle atrophy is a frequent complication of chronic kidney disease (CKD) and is associated with increased morbidity and mortality. The processes causing loss of muscle mass are also present in several catabolic conditions. Understanding the pathogenesis of CKD-induced muscle loss could lead to therapeutic interventions that prevent muscle wasting in CKD and potentially, other catabolic conditions. MAJOR

findingsInsulin or IGF-1 resistance caused by CKD, acidosis, inflammation, glucocorticoids or cancer causes defects in insulin-stimulated intracellular signaling that suppresses IRS-1 activity leading to decreased phosphorylation of Akt (p-Akt). A low p-Akt activates caspase-3 which provides muscle proteins substrates of the ubiquitin-proteasome system (UPS). A low p-Akt also leads to decreased phosphorylation of forkhead transcription factors which enter the nucleus to stimulate the expression of atrogin-1/MAFbx and MuRF1, E3 ubiquitin ligases that can be associated with proteolysis of muscle cells by the UPS. Caspase-3 also stimulates proteasome-dependent proteolysis in muscle. SUMMARY: In CKD, diabetes, inflammatory conditions or in response to acidosis or excess glucocorticoids, insulin resistance develops, initiating reduced IRS-1/PI3K/Akt signaling. In CKD, this reduces p-Akt which stimulates muscle proteolysis by activating caspase-3 and the UPS. Second, caspase-3 cleaves actomyosin yielding substrates for the UPS and increased proteasome-mediated proteolysis. Third, p-Akt down-regulation suppresses myogenesis in CKD. Fourth, exercise in CKD stimulates insulin/IGF-1 signaling to reduce muscle atrophy. Lastly, there is evidence that microRNAs influence insulin signaling providing a potential opportunity to design therapeutic interventions. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.

Indexed as

AnimalsHumansInsulin-Like Growth Factor IMetabolismMuscle, SkeletalMuscular AtrophyPhosphorylationRenal InsufficiencySignal TransductionInsulin-Like Growth Factor IAcidosisCancerDiabetesInflammation and glucocorticoid excessKidney failure

Identifiers

PMID23872437
PMCPMC3919551
OpenAlexW2016344437

What OpenQuestion holds

Textmetadata
LicenceTDM
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.