Evidence map›Paper›PMID 24981816›Full record

ReviewNature reviews. Nephrology2014

Mechanisms of muscle wasting in chronic kidney disease.

Xiaonan H Wang, William E Mitch

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 333 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
333citing papers in PubMed, 9 pooled it
13.1field-weighted citation impact, top 1% 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

333 citing papers in PubMed, 9 syntheses or guidelines pooled it, 587 citations in OpenAlex.

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  16. Muscle mass and plasma myostatin after exercise training: a substudy of Renal Exercise (RENEXC)-a randomized controlled trial.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021
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273 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 2 institutions in 1 country.

Xiaonan H WangRenal Division, Department of Medicine, Emory University, 1639 Pierce Drive, WMB 338, Atlanta, GA 30322, USA.
William E MitchNephrology Division, Department of Medicine, Baylor College of Medicine, One Baylor Plaza, ABBR R705, Houston, TX 77030, USA.
Baylor College of Medicine · USEmory University · US

Funding

PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR01DK037175 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Zhaoyong Hu · 1986 to 2026
$4.3M
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 R01 DK037175NIDDK NIH HHS R37 DK037175
6 · The paper itself

Abstract

In patients with chronic kidney disease (CKD), loss of cellular proteins increases the risks of morbidity and mortality. Persistence of muscle protein catabolism in CKD results in striking losses of muscle proteins as whole-body protein turnover is great; even small but persistent imbalances between protein synthesis and degradation cause substantial protein loss. No reliable methods to prevent CKD-induced muscle wasting currently exist, but mechanisms that control cellular protein turnover have been identified, suggesting that therapeutic strategies will be developed to suppress or block protein loss. Catabolic pathways that cause protein wasting include activation of the ubiquitin-proteasome system (UPS), caspase-3, lysosomes and myostatin (a negative regulator of skeletal muscle growth). These pathways can be initiated by complications associated with CKD, such as metabolic acidosis, defective insulin signalling, inflammation, increased angiotensin II levels, abnormal appetite regulation and impaired microRNA responses. Inflammation stimulates cellular signalling pathways that activate myostatin, which accelerates UPS-mediated catabolism. Blocking this pathway can prevent loss of muscle proteins. Myostatin inhibition could yield new therapeutic directions for blocking muscle protein wasting in CKD or disorders associated with its complications.

Indexed as

HomeostasisProtein BiosynthesisProteolysisHumansMuscle, SkeletalMuscular AtrophyRenal Insufficiency, ChronicSignal Transduction

Identifiers

PMID24981816
PMCPMC4269363
OpenAlexW1996025648

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.