Evidence map›Paper›PMID 32982782›Full record

ReviewFrontiers in physiology2020

The Impact of Immune Cells on the Skeletal Muscle Microenvironment During Cancer Cachexia.

Brandon N VanderVeen, E Angela Murphy, James A Carson

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
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

49 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Observational
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Hallmarks of Cancer Cachexia: Sexual Dimorphism in Related Pathways.International journal of molecular sciences · 2025
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Brandon N VanderVeenDepartment of Pathology, Microbiology, and Immunology, School of Medicine, University of South Carolina, Columbia, SC, United States.
E Angela MurphyDepartment of Pathology, Microbiology, and Immunology, School of Medicine, University of South Carolina, Columbia, SC, United States.
James A CarsonIntegrative Muscle Biology Laboratory, Division of Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, TN, United States.
University of South Carolina · USUniversity of Tennessee Health Science Center · US

Funding

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
Emodin as a chemopreventive agent for breast cancer - admin suppR01CA218578 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI FAN, DAPING, MURPHY, ELIZABETH ANGELA · 2018 to 2022
$1.9M
(PQ 12) The Regulation of Physical Function and Skeletal Muscle Metabolic Signaling After Cessation of 5-Fluorouracil TreatmentR21CA231131 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CARSON, JAMES A · 2019 to 2020
$342k
Emodin as a complementary dietary therapy to reduce toxicity of 5 fluorouracilR41AT009964 · NCCIH · ACEPRE, LLC · PI MURPHY, ELIZABETH ANGELA · 2018 to 2019
$300k
NCCIH NIH HHS R41 AT009964NCI NIH HHS R01 CA121249NCI NIH HHS R01 CA218578NCI NIH HHS R21 CA231131
6 · The paper itself

Abstract

Progressive weight loss combined with skeletal muscle atrophy, termed cachexia, is a common comorbidity associated with cancer that results in adverse consequences for the patient related to decreased chemotherapy responsiveness and increased mortality. Cachexia's complexity has provided a barrier for developing successful therapies to prevent or treat the condition, since a large number of systemic disruptions that can regulate muscle mass are often present. Furthermore, considerable effort has focused on investigating how tumor derived factors and inflammatory mediators directly signal skeletal muscle to disrupt protein turnover regulation. Currently, there is developing appreciation for understanding how cancer alters skeletal muscle's complex microenvironment and the tightly regulated interactions between multiple cell types. Skeletal muscle microenvironment interactions have established functions in muscle response to regeneration from injury, growth, aging, overload-induced hypertrophy, and exercise. This review explores the growing body of evidence for immune cell modulation of the skeletal muscle microenvironment during cancer-induced muscle wasting. Emphasis is placed on the regulatory network that integrates physiological responses between immune cells with other muscle cell types including satellite cells, fibroblast cells, and endothelial cells to regulate myofiber size and plasticity. The overall goal of this review is to provide an understanding of how different cell types that constitute the muscle microenvironment and their signaling mediators contribute to cancer and chemotherapy-induced muscle wasting.

Indexed as

endotheliumextracellular matrixfibroblastmacrophagesatellite cell

Identifiers

PMID32982782
PMCPMC7489038
OpenAlexW3082760569

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.