Cellular senescence in skeletal disease: mechanisms and treatment

Abstract 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 intervert...

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Main Authors: Xu He, Wei Hu, Yuanshu Zhang, Mimi Chen, Yicheng Ding, Huilin Yang, Fan He, Qiaoli Gu, Qin Shi
Format: Article
Language:English
Published: BMC 2023-10-01
Series:Cellular & Molecular Biology Letters
Subjects:
Online Access:https://doi.org/10.1186/s11658-023-00501-5
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author Xu He
Wei Hu
Yuanshu Zhang
Mimi Chen
Yicheng Ding
Huilin Yang
Fan He
Qiaoli Gu
Qin Shi
author_facet Xu He
Wei Hu
Yuanshu Zhang
Mimi Chen
Yicheng Ding
Huilin Yang
Fan He
Qiaoli Gu
Qin Shi
author_sort Xu He
collection DOAJ
description Abstract 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
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spelling doaj.art-5c429e3df2c24874a330716c1d3bd1572023-10-29T12:30:20ZengBMCCellular & Molecular Biology Letters1689-13922023-10-0128112010.1186/s11658-023-00501-5Cellular senescence in skeletal disease: mechanisms and treatmentXu He0Wei Hu1Yuanshu Zhang2Mimi Chen3Yicheng Ding4Huilin Yang5Fan He6Qiaoli Gu7Qin Shi8Department of Orthopedics, The First Affiliated Hospital of Soochow University, Orthopedic Institute of Soochow University, Medical College of Soochow UniversityDepartment of Orthopedics, The First Affiliated Hospital of Soochow University, Orthopedic Institute of Soochow University, Medical College of Soochow UniversityDepartment of Orthopedics, Wuxi Ninth People’s Hospital Affiliated to Soochow UniversityDepartment of Orthopedics, Children Hospital of Soochow UniversityXuzhou Medical UniversityDepartment of Orthopedics, The First Affiliated Hospital of Soochow University, Orthopedic Institute of Soochow University, Medical College of Soochow UniversityDepartment of Orthopedics, The First Affiliated Hospital of Soochow University, Orthopedic Institute of Soochow University, Medical College of Soochow UniversityDepartment of Orthopedics, The First Affiliated Hospital of Soochow University, Orthopedic Institute of Soochow University, Medical College of Soochow UniversityDepartment of Orthopedics, The First Affiliated Hospital of Soochow University, Orthopedic Institute of Soochow University, Medical College of Soochow UniversityAbstract 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 Abstracthttps://doi.org/10.1186/s11658-023-00501-5Cellular senescenceChronic inflammationAge-related orthopaedic diseasesSignalling pathwaysBone marrow
spellingShingle Xu He
Wei Hu
Yuanshu Zhang
Mimi Chen
Yicheng Ding
Huilin Yang
Fan He
Qiaoli Gu
Qin Shi
Cellular senescence in skeletal disease: mechanisms and treatment
Cellular & Molecular Biology Letters
Cellular senescence
Chronic inflammation
Age-related orthopaedic diseases
Signalling pathways
Bone marrow
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 Cellular senescence
Chronic inflammation
Age-related orthopaedic diseases
Signalling pathways
Bone marrow
url https://doi.org/10.1186/s11658-023-00501-5
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AT yichengding cellularsenescenceinskeletaldiseasemechanismsandtreatment
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