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Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia

Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostas...

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Autores principales: Molfino, Alessio, Gioia, Gianfranco, Fanelli, Filippo Rossi, Laviano, Alessandro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609516/
https://www.ncbi.nlm.nih.gov/pubmed/26504362
http://dx.doi.org/10.1155/2015/801685
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author Molfino, Alessio
Gioia, Gianfranco
Fanelli, Filippo Rossi
Laviano, Alessandro
author_facet Molfino, Alessio
Gioia, Gianfranco
Fanelli, Filippo Rossi
Laviano, Alessandro
author_sort Molfino, Alessio
collection PubMed
description Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostasis contribute to the onset of anorexia, reduced food intake, and increased catabolism of muscle mass and adipose tissue. In particular, functional changes are associated with increased hypothalamic concentration of proinflammatory cytokines, which suggests that neuroinflammation may represent the adaptive response of the brain to peripheral challenges, including tumor growth. Within this conceptual framework, the vagus nerve appears to be involved in conveying alert signals to the hypothalamus, whereas hypothalamic serotonin appears to contribute to triggering catabolic signals.
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spelling pubmed-46095162015-10-26 Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia Molfino, Alessio Gioia, Gianfranco Fanelli, Filippo Rossi Laviano, Alessandro Mediators Inflamm Review Article Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostasis contribute to the onset of anorexia, reduced food intake, and increased catabolism of muscle mass and adipose tissue. In particular, functional changes are associated with increased hypothalamic concentration of proinflammatory cytokines, which suggests that neuroinflammation may represent the adaptive response of the brain to peripheral challenges, including tumor growth. Within this conceptual framework, the vagus nerve appears to be involved in conveying alert signals to the hypothalamus, whereas hypothalamic serotonin appears to contribute to triggering catabolic signals. Hindawi Publishing Corporation 2015 2015-10-04 /pmc/articles/PMC4609516/ /pubmed/26504362 http://dx.doi.org/10.1155/2015/801685 Text en Copyright © 2015 Alessio Molfino et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Molfino, Alessio
Gioia, Gianfranco
Fanelli, Filippo Rossi
Laviano, Alessandro
Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia
title Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia
title_full Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia
title_fullStr Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia
title_full_unstemmed Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia
title_short Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia
title_sort contribution of neuroinflammation to the pathogenesis of cancer cachexia
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609516/
https://www.ncbi.nlm.nih.gov/pubmed/26504362
http://dx.doi.org/10.1155/2015/801685
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