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RAGE in the pathophysiology of skeletal muscle

Emerging evidence suggests that the signalling of the Receptor for Advanced Glycation End products (RAGE) is critical for skeletal muscle physiology controlling both the activity of muscle precursors during skeletal muscle development and the correct time of muscle regeneration after acute injury. O...

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Detalles Bibliográficos
Autores principales: Riuzzi, Francesca, Sorci, Guglielmo, Sagheddu, Roberta, Chiappalupi, Sara, Salvadori, Laura, Donato, Rosario
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6351676/
https://www.ncbi.nlm.nih.gov/pubmed/30334619
http://dx.doi.org/10.1002/jcsm.12350
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author Riuzzi, Francesca
Sorci, Guglielmo
Sagheddu, Roberta
Chiappalupi, Sara
Salvadori, Laura
Donato, Rosario
author_facet Riuzzi, Francesca
Sorci, Guglielmo
Sagheddu, Roberta
Chiappalupi, Sara
Salvadori, Laura
Donato, Rosario
author_sort Riuzzi, Francesca
collection PubMed
description Emerging evidence suggests that the signalling of the Receptor for Advanced Glycation End products (RAGE) is critical for skeletal muscle physiology controlling both the activity of muscle precursors during skeletal muscle development and the correct time of muscle regeneration after acute injury. On the other hand, the aberrant re‐expression/activity of RAGE in adult skeletal muscle is a hallmark of muscle wasting that occurs in response to ageing, genetic disorders, inflammatory conditions, cancer, and metabolic alterations. In this review, we discuss the mechanisms of action and the ligands of RAGE involved in myoblast differentiation, muscle regeneration, and muscle pathological conditions. We highlight potential therapeutic strategies for targeting RAGE to improve skeletal muscle function.
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spelling pubmed-63516762019-02-06 RAGE in the pathophysiology of skeletal muscle Riuzzi, Francesca Sorci, Guglielmo Sagheddu, Roberta Chiappalupi, Sara Salvadori, Laura Donato, Rosario J Cachexia Sarcopenia Muscle Reviews Emerging evidence suggests that the signalling of the Receptor for Advanced Glycation End products (RAGE) is critical for skeletal muscle physiology controlling both the activity of muscle precursors during skeletal muscle development and the correct time of muscle regeneration after acute injury. On the other hand, the aberrant re‐expression/activity of RAGE in adult skeletal muscle is a hallmark of muscle wasting that occurs in response to ageing, genetic disorders, inflammatory conditions, cancer, and metabolic alterations. In this review, we discuss the mechanisms of action and the ligands of RAGE involved in myoblast differentiation, muscle regeneration, and muscle pathological conditions. We highlight potential therapeutic strategies for targeting RAGE to improve skeletal muscle function. John Wiley and Sons Inc. 2018-10-18 2018-12 /pmc/articles/PMC6351676/ /pubmed/30334619 http://dx.doi.org/10.1002/jcsm.12350 Text en © 2018 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Reviews
Riuzzi, Francesca
Sorci, Guglielmo
Sagheddu, Roberta
Chiappalupi, Sara
Salvadori, Laura
Donato, Rosario
RAGE in the pathophysiology of skeletal muscle
title RAGE in the pathophysiology of skeletal muscle
title_full RAGE in the pathophysiology of skeletal muscle
title_fullStr RAGE in the pathophysiology of skeletal muscle
title_full_unstemmed RAGE in the pathophysiology of skeletal muscle
title_short RAGE in the pathophysiology of skeletal muscle
title_sort rage in the pathophysiology of skeletal muscle
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6351676/
https://www.ncbi.nlm.nih.gov/pubmed/30334619
http://dx.doi.org/10.1002/jcsm.12350
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