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The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis

Bones are constantly exposed to mechanical forces from both muscles and Earth’s gravity to maintain bone homeostasis by stimulating bone formation. Mechanotransduction transforms external mechanical signals such as force, fluid flow shear, and gravity into intracellular responses to achieve force ad...

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Detalles Bibliográficos
Autores principales: Liu, Zhaoshuo, Wang, Qilin, Zhang, Junyou, Qi, Sihan, Duan, Yingying, Li, Chunyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10532275/
https://www.ncbi.nlm.nih.gov/pubmed/37762629
http://dx.doi.org/10.3390/ijms241814326
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author Liu, Zhaoshuo
Wang, Qilin
Zhang, Junyou
Qi, Sihan
Duan, Yingying
Li, Chunyan
author_facet Liu, Zhaoshuo
Wang, Qilin
Zhang, Junyou
Qi, Sihan
Duan, Yingying
Li, Chunyan
author_sort Liu, Zhaoshuo
collection PubMed
description Bones are constantly exposed to mechanical forces from both muscles and Earth’s gravity to maintain bone homeostasis by stimulating bone formation. Mechanotransduction transforms external mechanical signals such as force, fluid flow shear, and gravity into intracellular responses to achieve force adaptation. However, the underlying molecular mechanisms on the conversion from mechanical signals into bone formation has not been completely defined yet. In the present review, we provide a comprehensive and systematic description of the mechanotransduction signaling pathways induced by mechanical stimuli during osteogenesis and address the different layers of interconnections between different signaling pathways. Further exploration of mechanotransduction would benefit patients with osteoporosis, including the aging population and postmenopausal women.
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spelling pubmed-105322752023-09-28 The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis Liu, Zhaoshuo Wang, Qilin Zhang, Junyou Qi, Sihan Duan, Yingying Li, Chunyan Int J Mol Sci Review Bones are constantly exposed to mechanical forces from both muscles and Earth’s gravity to maintain bone homeostasis by stimulating bone formation. Mechanotransduction transforms external mechanical signals such as force, fluid flow shear, and gravity into intracellular responses to achieve force adaptation. However, the underlying molecular mechanisms on the conversion from mechanical signals into bone formation has not been completely defined yet. In the present review, we provide a comprehensive and systematic description of the mechanotransduction signaling pathways induced by mechanical stimuli during osteogenesis and address the different layers of interconnections between different signaling pathways. Further exploration of mechanotransduction would benefit patients with osteoporosis, including the aging population and postmenopausal women. MDPI 2023-09-20 /pmc/articles/PMC10532275/ /pubmed/37762629 http://dx.doi.org/10.3390/ijms241814326 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Liu, Zhaoshuo
Wang, Qilin
Zhang, Junyou
Qi, Sihan
Duan, Yingying
Li, Chunyan
The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis
title The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis
title_full The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis
title_fullStr The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis
title_full_unstemmed The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis
title_short The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis
title_sort mechanotransduction signaling pathways in the regulation of osteogenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10532275/
https://www.ncbi.nlm.nih.gov/pubmed/37762629
http://dx.doi.org/10.3390/ijms241814326
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