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Abstract
Cellular senescence and the senescence-associated secretory phenotype (SASP) are linked to bone remodelling impairment in ageing.
- Senescent cells in the bone microenvironment secrete factors that promote inflammation and disrupt normal bone repair.
- These factors, including pro-inflammatory cytokines and Wnt antagonists like sclerostin, converge on critical biological pathways affecting bone health.
- Clearing senescent cells has shown potential in preventing age-related bone loss in mice.
- The SASP may act as a significant contributor to skeletal ageing, distinct from traditional pathways of bone deterioration.
- Differential profiles of the SASP components are observed in age-related, postmenopausal, and secondary osteoporosis.
- Future research should prioritize the validation of biomarkers and evaluate long-term outcomes of senolytic and senomorphic treatments.
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