Cargando…

Cellular and molecular mechanisms of sarcopenia: the S100B perspective

Primary sarcopenia is a condition of reduced skeletal muscle mass and strength, reduced agility, and increased fatigability and risk of bone fractures characteristic of aged, otherwise healthy people. The pathogenesis of primary sarcopenia is not completely understood. Herein, we review the essentia...

Descripción completa

Detalles Bibliográficos
Autores principales: Riuzzi, Francesca, Sorci, Guglielmo, Arcuri, Cataldo, Giambanco, Ileana, Bellezza, Ilaria, Minelli, Alba, 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/PMC6351675/
https://www.ncbi.nlm.nih.gov/pubmed/30499235
http://dx.doi.org/10.1002/jcsm.12363
_version_ 1783390630110560256
author Riuzzi, Francesca
Sorci, Guglielmo
Arcuri, Cataldo
Giambanco, Ileana
Bellezza, Ilaria
Minelli, Alba
Donato, Rosario
author_facet Riuzzi, Francesca
Sorci, Guglielmo
Arcuri, Cataldo
Giambanco, Ileana
Bellezza, Ilaria
Minelli, Alba
Donato, Rosario
author_sort Riuzzi, Francesca
collection PubMed
description Primary sarcopenia is a condition of reduced skeletal muscle mass and strength, reduced agility, and increased fatigability and risk of bone fractures characteristic of aged, otherwise healthy people. The pathogenesis of primary sarcopenia is not completely understood. Herein, we review the essentials of the cellular and molecular mechanisms of skeletal mass maintenance; the alterations of myofiber metabolism and deranged properties of muscle satellite cells (the adult stem cells of skeletal muscles) that underpin the pathophysiology of primary sarcopenia; the role of the Ca(2+)‐sensor protein, S100B, as an intracellular factor and an extracellular signal regulating cell functions; and the functional role of S100B in muscle tissue. Lastly, building on recent results pointing to S100B as to a molecular determinant of myoblast–brown adipocyte transition, we propose S100B as a transducer of the deleterious effects of accumulation of reactive oxygen species in myoblasts and, potentially, myofibers concurring to the pathophysiology of sarcopenia.
format Online
Article
Text
id pubmed-6351675
institution National Center for Biotechnology Information
language English
publishDate 2018
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-63516752019-02-06 Cellular and molecular mechanisms of sarcopenia: the S100B perspective Riuzzi, Francesca Sorci, Guglielmo Arcuri, Cataldo Giambanco, Ileana Bellezza, Ilaria Minelli, Alba Donato, Rosario J Cachexia Sarcopenia Muscle Reviews Primary sarcopenia is a condition of reduced skeletal muscle mass and strength, reduced agility, and increased fatigability and risk of bone fractures characteristic of aged, otherwise healthy people. The pathogenesis of primary sarcopenia is not completely understood. Herein, we review the essentials of the cellular and molecular mechanisms of skeletal mass maintenance; the alterations of myofiber metabolism and deranged properties of muscle satellite cells (the adult stem cells of skeletal muscles) that underpin the pathophysiology of primary sarcopenia; the role of the Ca(2+)‐sensor protein, S100B, as an intracellular factor and an extracellular signal regulating cell functions; and the functional role of S100B in muscle tissue. Lastly, building on recent results pointing to S100B as to a molecular determinant of myoblast–brown adipocyte transition, we propose S100B as a transducer of the deleterious effects of accumulation of reactive oxygen species in myoblasts and, potentially, myofibers concurring to the pathophysiology of sarcopenia. John Wiley and Sons Inc. 2018-11-30 2018-12 /pmc/articles/PMC6351675/ /pubmed/30499235 http://dx.doi.org/10.1002/jcsm.12363 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-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Reviews
Riuzzi, Francesca
Sorci, Guglielmo
Arcuri, Cataldo
Giambanco, Ileana
Bellezza, Ilaria
Minelli, Alba
Donato, Rosario
Cellular and molecular mechanisms of sarcopenia: the S100B perspective
title Cellular and molecular mechanisms of sarcopenia: the S100B perspective
title_full Cellular and molecular mechanisms of sarcopenia: the S100B perspective
title_fullStr Cellular and molecular mechanisms of sarcopenia: the S100B perspective
title_full_unstemmed Cellular and molecular mechanisms of sarcopenia: the S100B perspective
title_short Cellular and molecular mechanisms of sarcopenia: the S100B perspective
title_sort cellular and molecular mechanisms of sarcopenia: the s100b perspective
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6351675/
https://www.ncbi.nlm.nih.gov/pubmed/30499235
http://dx.doi.org/10.1002/jcsm.12363
work_keys_str_mv AT riuzzifrancesca cellularandmolecularmechanismsofsarcopeniathes100bperspective
AT sorciguglielmo cellularandmolecularmechanismsofsarcopeniathes100bperspective
AT arcuricataldo cellularandmolecularmechanismsofsarcopeniathes100bperspective
AT giambancoileana cellularandmolecularmechanismsofsarcopeniathes100bperspective
AT bellezzailaria cellularandmolecularmechanismsofsarcopeniathes100bperspective
AT minellialba cellularandmolecularmechanismsofsarcopeniathes100bperspective
AT donatorosario cellularandmolecularmechanismsofsarcopeniathes100bperspective