Cellular senescence in skeletal disease: mechanisms and treatment.
Age-related orthopaedic diseases
Bone marrow
Cellular senescence
Chronic inflammation
Signalling pathways
Journal
Cellular & molecular biology letters
ISSN: 1689-1392
Titre abrégé: Cell Mol Biol Lett
Pays: England
ID NLM: 9607427
Informations de publication
Date de publication:
27 Oct 2023
27 Oct 2023
Historique:
received:
19
05
2023
accepted:
12
10
2023
medline:
30
10
2023
pubmed:
28
10
2023
entrez:
27
10
2023
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 37891477
doi: 10.1186/s11658-023-00501-5
pii: 10.1186/s11658-023-00501-5
pmc: PMC10612178
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
88Subventions
Organisme : National Natural Science Foundation of China
ID : 82172485
Informations de copyright
© 2023. The Author(s).
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