Evidence map›Paper›PMID 27486747›Full record

ArticlePloS one2016

Skeletal Muscle Regeneration and Oxidative Stress Are Altered in Chronic Kidney Disease.

Keith G Avin, Neal X Chen, Jason M Organ, Chad Zarse, Kalisha O'Neill, Richard G Conway, Robert J Konrad, Robert L Bacallao, Matthew R Allen, Sharon M Moe

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
3.3field-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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Review
  5. Article
  6. Zinc deficiency contributes to blunted myogenesis in chronic kidney disease.American journal of physiology. Cell physiology · 2026
    Article
  7. Article
  8. Article
  9. Review
  10. Article
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  12. Article
  13. Article
  14. American journal of physiology. Renal physiology · 2023
    Article
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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

10 authors at 2 institutions in 1 country.

Keith G AvinDepartment of Physical Therapy, Indiana University School of Health and Rehabilitation Sciences, Indianapolis, IN, United States of America.ORCID http://orcid.org/0000-0001-9426-7862
Neal X ChenDivision of Nephrology, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Jason M OrganDepartment of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Chad ZarseDivision of Nephrology, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Kalisha O'NeillDivision of Nephrology, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Richard G ConwayLilly Research laboratories, Eli Lilly and Company, Indianapolis, IN, United States of America.
Robert J KonradLilly Research laboratories, Eli Lilly and Company, Indianapolis, IN, United States of America.
Robert L BacallaoDivision of Nephrology, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Matthew R AllenDepartment of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Sharon M MoeDivision of Nephrology, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Indiana University School of MedicineEli Lilly (United States) · US

Funding

Bisphosphonates in the treatment of chronic kidney disease-mineral bone diseaseR01AR058005 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI MOE, SHARON M · 2010 to 2014
$1.6M
Mechanisms of Interventions to Ameliorate Sarcopenia in Chronic Kidney DiseaseK08DK110429 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI AVIN, KEITH G · 2016 to 2021
$718k
NIAMS NIH HHS R01 AR058005NIDDK NIH HHS K08 DK110429
6 · The paper itself

Abstract

Skeletal muscle atrophy and impaired muscle function are associated with lower health-related quality of life, and greater disability and mortality risk in those with chronic kidney disease (CKD). However, the pathogenesis of skeletal dysfunction in CKD is unknown. We used a slow progressing, naturally occurring, CKD rat model (Cy/+ rat) with hormonal abnormalities consistent with clinical presentations of CKD to study skeletal muscle signaling. The CKD rats demonstrated augmented skeletal muscle regeneration with higher activation and differentiation signals in muscle cells (i.e. lower Pax-7; higher MyoD and myogenin RNA expression). However, there was also higher expression of proteolytic markers (Atrogin-1 and MuRF-1) in CKD muscle relative to normal. CKD animals had higher indices of oxidative stress compared to normal, evident by elevated plasma levels of an oxidative stress marker, 8-hydroxy-2' -deoxyguanosine (8-OHdG), increased muscle expression of succinate dehydrogenase (SDH) and Nox4 and altered mitochondria morphology. Furthermore, we show significantly higher serum levels of myostatin and expression of myostatin in skeletal muscle of CKD animals compared to normal. Taken together, these data show aberrant regeneration and proteolytic signaling that is associated with oxidative stress and high levels of myostatin in the setting of CKD. These changes likely play a role in the compromised skeletal muscle function that exists in CKD.

Indexed as

AnimalsCell DifferentiationDisease Models, AnimalHumansMaleMuscle, SkeletalMyostatinOxidative StressRatsRegenerationRenal Insufficiency, ChronicSignal TransductionMstn protein, ratMyostatin

Identifiers

PMID27486747
PMCPMC4972446
OpenAlexW2491375235

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.