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Cellular senescence in skeletal disease: mechanisms and treatment

The musculoskeletal system supports the movement of the entire body and provides blood production while acting as an endocrine organ. With aging, the balance of bone homeostasis is disrupted, leading to bone loss and degenerative diseases, such as osteoporosis, osteoarthritis, and intervertebral dis...

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Autores principales: He, Xu, Hu, Wei, Zhang, Yuanshu, Chen, Mimi, Ding, Yicheng, Yang, Huilin, He, Fan, Gu, Qiaoli, Shi, Qin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10612178/
https://www.ncbi.nlm.nih.gov/pubmed/37891477
http://dx.doi.org/10.1186/s11658-023-00501-5
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author He, Xu
Hu, Wei
Zhang, Yuanshu
Chen, Mimi
Ding, Yicheng
Yang, Huilin
He, Fan
Gu, Qiaoli
Shi, Qin
author_facet He, Xu
Hu, Wei
Zhang, Yuanshu
Chen, Mimi
Ding, Yicheng
Yang, Huilin
He, Fan
Gu, Qiaoli
Shi, Qin
author_sort He, Xu
collection PubMed
description The musculoskeletal system supports the movement of the entire body and provides blood production while acting as an endocrine organ. With aging, the balance of bone homeostasis is disrupted, leading to bone loss and degenerative diseases, such as osteoporosis, osteoarthritis, and intervertebral disc degeneration. Skeletal diseases have a profound impact on the motor and cognitive abilities of the elderly, thus creating a major challenge for both global health and the economy. Cellular senescence is caused by various genotoxic stressors and results in permanent cell cycle arrest, which is considered to be the underlying mechanism of aging. During aging, senescent cells (SnCs) tend to aggregate in the bone and trigger chronic inflammation by releasing senescence-associated secretory phenotypic factors. Multiple signalling pathways are involved in regulating cellular senescence in bone and bone marrow microenvironments. Targeted SnCs alleviate age-related degenerative diseases. However, the association between senescence and age-related diseases remains unclear. This review summarises the fundamental role of senescence in age-related skeletal diseases, highlights the signalling pathways that mediate senescence, and discusses potential therapeutic strategies for targeting SnCs. GRAPHICAL ABSTRACT: [Image: see text]
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spelling pubmed-106121782023-10-29 Cellular senescence in skeletal disease: mechanisms and treatment He, Xu Hu, Wei Zhang, Yuanshu Chen, Mimi Ding, Yicheng Yang, Huilin He, Fan Gu, Qiaoli Shi, Qin Cell Mol Biol Lett Mini Review The musculoskeletal system supports the movement of the entire body and provides blood production while acting as an endocrine organ. With aging, the balance of bone homeostasis is disrupted, leading to bone loss and degenerative diseases, such as osteoporosis, osteoarthritis, and intervertebral disc degeneration. Skeletal diseases have a profound impact on the motor and cognitive abilities of the elderly, thus creating a major challenge for both global health and the economy. Cellular senescence is caused by various genotoxic stressors and results in permanent cell cycle arrest, which is considered to be the underlying mechanism of aging. During aging, senescent cells (SnCs) tend to aggregate in the bone and trigger chronic inflammation by releasing senescence-associated secretory phenotypic factors. Multiple signalling pathways are involved in regulating cellular senescence in bone and bone marrow microenvironments. Targeted SnCs alleviate age-related degenerative diseases. However, the association between senescence and age-related diseases remains unclear. This review summarises the fundamental role of senescence in age-related skeletal diseases, highlights the signalling pathways that mediate senescence, and discusses potential therapeutic strategies for targeting SnCs. GRAPHICAL ABSTRACT: [Image: see text] BioMed Central 2023-10-27 /pmc/articles/PMC10612178/ /pubmed/37891477 http://dx.doi.org/10.1186/s11658-023-00501-5 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Mini Review
He, Xu
Hu, Wei
Zhang, Yuanshu
Chen, Mimi
Ding, Yicheng
Yang, Huilin
He, Fan
Gu, Qiaoli
Shi, Qin
Cellular senescence in skeletal disease: mechanisms and treatment
title Cellular senescence in skeletal disease: mechanisms and treatment
title_full Cellular senescence in skeletal disease: mechanisms and treatment
title_fullStr Cellular senescence in skeletal disease: mechanisms and treatment
title_full_unstemmed Cellular senescence in skeletal disease: mechanisms and treatment
title_short Cellular senescence in skeletal disease: mechanisms and treatment
title_sort cellular senescence in skeletal disease: mechanisms and treatment
topic Mini Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10612178/
https://www.ncbi.nlm.nih.gov/pubmed/37891477
http://dx.doi.org/10.1186/s11658-023-00501-5
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