Evidence map›Paper›PMID 26054539›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

CKD Stimulates Muscle Protein Loss Via Rho-associated Protein Kinase 1 Activation.

Hui Peng, Jin Cao, Rizhen Yu, Farhad Danesh, Yanlin Wang, William E Mitch, Jing Xu, Zhaoyong Hu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Hui PengDepartment of Internal Medicine, Nephrology Division, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China; Nephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas;
Jin CaoNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas;
Rizhen YuNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas; Renal Section, Changhai Hospital, Shanghai, China; and.
Farhad DaneshNephrology Division, University of Texas MD Anderson Cancer Center, Houston, Texas.
Yanlin WangNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas;
William E MitchNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas;
Jing XuNephrology Division, University of Texas MD Anderson Cancer Center, Houston, Texas zhaoyonh@bcm.edu xuj1010@126.com.
Zhaoyong HuNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas; zhaoyonh@bcm.edu xuj1010@126.com.
Baylor College of Medicine · USChanghai Hospital · CNThe University of Texas MD Anderson Cancer Center · USThird Affiliated Hospital of Sun Yat-sen University · CN

Funding

PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR37DK037175 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2006 to 2015
$3.8M
Cellular and Molecular Mechanisms of Renal FibrosisR01DK095835 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WANG, YANLIN · 2012 to 2021
$3.2M
Mechanisms of Protein-Energy-Wasting in Chronic Kidney DiseaseR01AR063686 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI HU, ZHAOYONG · 2013 to 2017
$1.7M
NIAMS NIH HHS 5R01-AR063686NIAMS NIH HHS R01 AR063686NIDDK NIH HHS R01 DK095835NIDDK NIH HHS R37 DK037175NIDDK NIH HHS R37-DK 37175
6 · The paper itself

Abstract

In patients with CKD, muscle wasting is common and is associated with morbidity and mortality. Mechanisms leading to loss of muscle proteins include insulin resistance, which suppresses Akt activity and thus stimulates protein degradation via the ubiquitin-proteasome system. However, the specific factors controlling CKD-induced suppression of Akt activity in muscle remain undefined. In mice with CKD, the reduction in Akt activity in muscle exceeded the decrease in upstream insulin receptor substrate-1-associated phosphatidylinositol 3-kinase activity, suggesting that CKD activates other pathways that suppress Akt. Furthermore, a CKD-induced increase uncovered caspase-3 activity in muscle in these mice. In C2C12 muscle cells, activated caspase-3 cleaves and activates Rho-associated protein kinase 1 (ROCK1), which enhances the activity of phosphatase and tensin homolog (PTEN) and reduces Akt activity. Notably, constitutive activation of ROCK1 also led to increased caspase-3 activity in vitro. In mice with either global ROCK1 knockout or muscle-specific PTEN knockout, CKD-associated muscle proteolysis was blunted. These results suggest ROCK1 activation in CKD and perhaps in other catabolic conditions can promote loss of muscle protein via a negative feedback loop.

Indexed as

AnimalsCaspase 3MaleMiceMuscle ProteinsPTEN PhosphohydrolaseRenal Insufficiency, Chronicrho-Associated KinasesCaspase 3Muscle ProteinsPTEN PhosphohydrolasePten protein, mouserho-Associated KinasesRock1 protein, mousecell signalingchronic kidney diseasemetabolism

Identifiers

PMID26054539
PMCPMC4731120
OpenAlexW1904021157

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.