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Molecular Basis of Bone Aging

A decline in bone mass leading to an increased fracture risk is a common feature of age-related bone changes. The mechanisms underlying bone senescence are very complex and implicate systemic and local factors and are the result of the combination of several changes occurring at the cellular, tissue...

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Detalles Bibliográficos
Autores principales: Corrado, Addolorata, Cici, Daniela, Rotondo, Cinzia, Maruotti, Nicola, Cantatore, Francesco Paolo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279376/
https://www.ncbi.nlm.nih.gov/pubmed/32456199
http://dx.doi.org/10.3390/ijms21103679
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author Corrado, Addolorata
Cici, Daniela
Rotondo, Cinzia
Maruotti, Nicola
Cantatore, Francesco Paolo
author_facet Corrado, Addolorata
Cici, Daniela
Rotondo, Cinzia
Maruotti, Nicola
Cantatore, Francesco Paolo
author_sort Corrado, Addolorata
collection PubMed
description A decline in bone mass leading to an increased fracture risk is a common feature of age-related bone changes. The mechanisms underlying bone senescence are very complex and implicate systemic and local factors and are the result of the combination of several changes occurring at the cellular, tissue and structural levels; they include alterations of bone cell differentiation and activity, oxidative stress, genetic damage and the altered responses of bone cells to various biological signals and to mechanical loading. The molecular mechanisms responsible for these changes remain greatly unclear and many data derived from in vitro or animal studies appear to be conflicting and heterogeneous, probably due to the different experimental approaches; nevertheless, understanding the main physio-pathological processes that cause bone senescence is essential for the development of new potential therapeutic options for treating age-related bone loss. This article reviews the current knowledge concerning the molecular mechanisms underlying the pathogenesis of age-related bone changes.
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spelling pubmed-72793762020-06-17 Molecular Basis of Bone Aging Corrado, Addolorata Cici, Daniela Rotondo, Cinzia Maruotti, Nicola Cantatore, Francesco Paolo Int J Mol Sci Review A decline in bone mass leading to an increased fracture risk is a common feature of age-related bone changes. The mechanisms underlying bone senescence are very complex and implicate systemic and local factors and are the result of the combination of several changes occurring at the cellular, tissue and structural levels; they include alterations of bone cell differentiation and activity, oxidative stress, genetic damage and the altered responses of bone cells to various biological signals and to mechanical loading. The molecular mechanisms responsible for these changes remain greatly unclear and many data derived from in vitro or animal studies appear to be conflicting and heterogeneous, probably due to the different experimental approaches; nevertheless, understanding the main physio-pathological processes that cause bone senescence is essential for the development of new potential therapeutic options for treating age-related bone loss. This article reviews the current knowledge concerning the molecular mechanisms underlying the pathogenesis of age-related bone changes. MDPI 2020-05-23 /pmc/articles/PMC7279376/ /pubmed/32456199 http://dx.doi.org/10.3390/ijms21103679 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
Corrado, Addolorata
Cici, Daniela
Rotondo, Cinzia
Maruotti, Nicola
Cantatore, Francesco Paolo
Molecular Basis of Bone Aging
title Molecular Basis of Bone Aging
title_full Molecular Basis of Bone Aging
title_fullStr Molecular Basis of Bone Aging
title_full_unstemmed Molecular Basis of Bone Aging
title_short Molecular Basis of Bone Aging
title_sort molecular basis of bone aging
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279376/
https://www.ncbi.nlm.nih.gov/pubmed/32456199
http://dx.doi.org/10.3390/ijms21103679
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