Evidence map›Paper›PMID 26593326›Full record

ReviewSeminars in cell & developmental biology2016

The emerging role of skeletal muscle oxidative metabolism as a biological target and cellular regulator of cancer-induced muscle wasting.

James A Carson, Justin P Hardee, Brandon N VanderVeen

Abstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Cancer Cachexia.Advances in experimental medicine and biology · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. UBR2 targets myosin heavy chain IIb and IIx for degradation: Molecular mechanism essential for cancer-induced muscle wasting.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article

11 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

3 authors at 1 institution in 1 country.

James A CarsonIntegrative Muscle Biology Laboratory, Department of Exercise Science, University of South Carolina, 921 Assembly St., Columbia, SC, 29208, USA. Electronic address: carsonj@mailbox.sc.edu.
Justin P HardeeIntegrative Muscle Biology Laboratory, Department of Exercise Science, University of South Carolina, 921 Assembly St., Columbia, SC, 29208, USA.
Brandon N VanderVeenIntegrative Muscle Biology Laboratory, Department of Exercise Science, University of South Carolina, 921 Assembly St., Columbia, SC, 29208, USA.
University of South Carolina · US

Funding

TISSUE BIOREPOSITORYP20RR017698 · NCRR · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI FAYAD, RAJA · 2002 to 2011
$22.5M
Cachexia in ApcMin/+ mice: The role of IL-6R01CA121249 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CARSON, JAMES A · 2008 to 2018
$2.7M
NCI NIH HHS R01 CA121249NCRR NIH HHS P20 RR017698
6 · The paper itself

Abstract

While skeletal muscle mass is an established primary outcome related to understanding cancer cachexia mechanisms, considerable gaps exist in our understanding of muscle biochemical and functional properties that have recognized roles in systemic health. Skeletal muscle quality is a classification beyond mass, and is aligned with muscle's metabolic capacity and substrate utilization flexibility. This supplies an additional role for the mitochondria in cancer-induced muscle wasting. While the historical assessment of mitochondria content and function during cancer-induced muscle loss was closely aligned with energy flux and wasting susceptibility, this understanding has expanded to link mitochondria dysfunction to cellular processes regulating myofiber wasting. The primary objective of this article is to highlight muscle mitochondria and oxidative metabolism as a biological target of cancer cachexia and also as a cellular regulator of cancer-induced muscle wasting. Initially, we examine the role of muscle metabolic phenotype and mitochondria content in cancer-induced wasting susceptibility. We then assess the evidence for cancer-induced regulation of skeletal muscle mitochondrial biogenesis, dynamics, mitophagy, and oxidative stress. In addition, we discuss environments associated with cancer cachexia that can impact the regulation of skeletal muscle oxidative metabolism. The article also examines the role of cytokine-mediated regulation of mitochondria function, followed by the potential role of cancer-induced hypogonadism. Lastly, a role for decreased muscle use in cancer-induced mitochondrial dysfunction is reviewed.

Indexed as

AnimalsCachexiaHumansMitochondriaModels, BiologicalMuscle, SkeletalNeoplasmsOxidation-ReductionCytokineDisuseHypogonadismMitochondria

Identifiers

PMID26593326
PMCPMC4867246
OpenAlexW2175296021

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.