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"Bone-SASP" in Skeletal Aging.
Ching-Lien Fang1, Bin Liu1, Mei Wan2,3
1Department of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Cellular senescence, marked by cell cycle arrest and the senescence-associated secretory phenotype (SASP), drives bone pathologies. Bone-SASP contributes to aging, premature aging syndromes, and osteoarthritis.
Area of Science:
- Cellular biology
- Gerontology
- Skeletal biology
Background:
- Cellular senescence is a state of stable cell cycle arrest.
- The senescence-associated secretory phenotype (SASP) involves the release of various factors.
- Senescent cells and their SASP contribute to age-associated disorders.
Purpose of the Study:
- To review the role of cellular senescence and SASP in bone pathologies.
- To focus on the impact of bone-SASP in aging and related conditions.
- To discuss the contribution of bone-SASP to osteoarthritis.
Main Methods:
- Literature review of cellular senescence and SASP.
- Focus on bone cell-associated SASP (bone-SASP).
- Analysis of bone-SASP's role in aging, premature aging syndromes, glucocorticoid-induced bone damage, and osteoarthritis.
Main Results:
- Senescent cells in bone produce SASP factors that alter skeletal structure via paracrine effects.
- Bone-SASP is implicated in natural and premature aging bone pathologies.
- Bone-SASP contributes to glucocorticoid-induced bone damage and osteoarthritis development.
Conclusions:
- Cellular senescence and bone-SASP are key mediators of bone pathologies.
- Bone-SASP plays a significant role in skeletal aging and disease.
- Understanding bone-SASP mechanisms is crucial for treating bone disorders.
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