Evidence map›Paper›PMID 27897418›Full record

ArticleJournal of cachexia, sarcopenia and muscle2017

Suppression of muscle wasting by the plant-derived compound ursolic acid in a model of chronic kidney disease.

Rizhen Yu, Ji-An Chen, Jing Xu, Jin Cao, Yanlin Wang, Sandhya S Thomas, Zhaoyong Hu

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 69 citations in OpenAlex.

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  19. Effects of Maca on Muscle Hypertrophy in C2C12 Skeletal Muscle Cells.International journal of molecular sciences · 2022
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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

7 authors at 3 institutions in 2 countries.

Rizhen YuNephrology Division, Changhai Hospital, Shanghai, China.
Ji-An ChenDepartment of Health Education, College of Preventive Medicine, Third Military Medical University, Chongqing, China.
Jing XuNephrology Division, Changhai Hospital, Shanghai, China.
Jin CaoNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Yanlin WangNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Sandhya S ThomasMichael E. Debakey VA Medical Center, Houston, TX, USA.
Zhaoyong HuNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Baylor College of Medicine · USSecond Military Medical University · CNArmy Medical University · CN

Funding

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
Chronic_Kidney_Disease_and_Impaired_Actions_of_InsulinIK2BX002492 · VA · MICHAEL E DEBAKEY VA MEDICAL CENTER · PI THOMAS, SANDHYA S · 2015 to 2019
–
BLRD VA IK2 BX002492NIAMS NIH HHS R01 AR063686NIDDK NIH HHS R01 DK095835
6 · The paper itself

Abstract

backgroundMuscle wasting in chronic kidney disease (CKD) and other catabolic disorders contributes to morbidity and mortality, and there are no therapeutic interventions that regularly and safely block losses of muscle mass. We have obtained evidence that impaired IGF-1/insulin signalling and increases in glucocorticoids, myostatin and/or inflammatory cytokines that contribute to the development of muscle wasting in catabolic disorders by activating protein degradation.

methodsUsing in vitro and in vivo models of muscle wasting associated with CKD or dexamethasone administration, we measured protein synthesis and degradation and examined mechanisms by which ursolic acid, derived from plants, could block the loss of muscle mass stimulated by CKD or excessive levels of dexamethasone.

resultsUsing cultured C2C12 myotubes to study muscle wasting, we found that exposure to glucocorticoids cause loss of cell proteins plus an increase in myostatin; both responses are significantly suppressed by ursolic acid. Results from promoter and ChIP assays demonstrated a mechanism involving ursolic acid blockade of myostatin promoter activity that is related to CEBP/δ expression. In mouse models of CKD-induced or dexamethasone-induced muscle wasting, we found that ursolic acid blocked the loss of muscle mass by stimulating protein synthesis and decreasing protein degradation. These beneficial responses included decreased expression of myostatin and inflammatory cytokines (e.g. TGF-β, IL-6 and TNFα), which are initiators of muscle-specific ubiquitin-E3 ligases (e.g. Atrogin-1, MuRF-1 and MUSA1).

conclusionsUrsolic acid improves CKD-induced muscle mass by suppressing the expression of myostatin and inflammatory cytokines via increasing protein synthesis and reducing proteolysis.

Indexed as

AnimalsCell LineCytokinesDexamethasoneDisease Models, AnimalMaleMice, Inbred C57BLMuscle Fibers, SkeletalMuscle, SkeletalMuscular AtrophyMyostatinProtein BiosynthesisProteolysisRenal Insufficiency, ChronicTriterpenesUrsolic AcidCytokinesDexamethasoneMstn protein, mouseMyostatinTriterpenesUrsolic AcidCachexiaChronic kidney diseaseMuscle wastingMyostatinUrsolic acid

Identifiers

PMID27897418
PMCPMC5377392
OpenAlexW2550722383

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.