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Cancer-Associated Muscle Wasting—Candidate Mechanisms and Molecular Pathways
Excessive muscle loss is commonly observed in cancer patients and its association with poor prognosis has been well-established. Cancer-associated sarcopenia differs from age-related wasting in that it is not responsive to nutritional intervention and exercise. This is related to its unique pathogen...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7729509/ https://www.ncbi.nlm.nih.gov/pubmed/33291708 http://dx.doi.org/10.3390/ijms21239268 |
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author | Armstrong, Victoria S. Fitzgerald, Liam W. Bathe, Oliver F. |
author_facet | Armstrong, Victoria S. Fitzgerald, Liam W. Bathe, Oliver F. |
author_sort | Armstrong, Victoria S. |
collection | PubMed |
description | Excessive muscle loss is commonly observed in cancer patients and its association with poor prognosis has been well-established. Cancer-associated sarcopenia differs from age-related wasting in that it is not responsive to nutritional intervention and exercise. This is related to its unique pathogenesis, a result of diverse and interconnected mechanisms including inflammation, disordered metabolism, proteolysis and autophagy. There is a growing body of evidence that suggests that the tumor is the driver of muscle wasting by its elaboration of mediators that influence each of these pro-sarcopenic pathways. In this review, evidence for these tumor-derived factors and putative mechanisms for inducing muscle wasting will be reviewed. Potential targets for future research and therapeutic interventions will also be reviewed. |
format | Online Article Text |
id | pubmed-7729509 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-77295092020-12-12 Cancer-Associated Muscle Wasting—Candidate Mechanisms and Molecular Pathways Armstrong, Victoria S. Fitzgerald, Liam W. Bathe, Oliver F. Int J Mol Sci Review Excessive muscle loss is commonly observed in cancer patients and its association with poor prognosis has been well-established. Cancer-associated sarcopenia differs from age-related wasting in that it is not responsive to nutritional intervention and exercise. This is related to its unique pathogenesis, a result of diverse and interconnected mechanisms including inflammation, disordered metabolism, proteolysis and autophagy. There is a growing body of evidence that suggests that the tumor is the driver of muscle wasting by its elaboration of mediators that influence each of these pro-sarcopenic pathways. In this review, evidence for these tumor-derived factors and putative mechanisms for inducing muscle wasting will be reviewed. Potential targets for future research and therapeutic interventions will also be reviewed. MDPI 2020-12-04 /pmc/articles/PMC7729509/ /pubmed/33291708 http://dx.doi.org/10.3390/ijms21239268 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Armstrong, Victoria S. Fitzgerald, Liam W. Bathe, Oliver F. Cancer-Associated Muscle Wasting—Candidate Mechanisms and Molecular Pathways |
title | Cancer-Associated Muscle Wasting—Candidate Mechanisms and Molecular Pathways |
title_full | Cancer-Associated Muscle Wasting—Candidate Mechanisms and Molecular Pathways |
title_fullStr | Cancer-Associated Muscle Wasting—Candidate Mechanisms and Molecular Pathways |
title_full_unstemmed | Cancer-Associated Muscle Wasting—Candidate Mechanisms and Molecular Pathways |
title_short | Cancer-Associated Muscle Wasting—Candidate Mechanisms and Molecular Pathways |
title_sort | cancer-associated muscle wasting—candidate mechanisms and molecular pathways |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7729509/ https://www.ncbi.nlm.nih.gov/pubmed/33291708 http://dx.doi.org/10.3390/ijms21239268 |
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