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Mechanisms of aging-related secretory phenotype regulation in osteoporosis: Network regulation, trade-offs and homeostasis
How aging-related cell secretions are controlled in osteoporosis: balancing network regulation and stability
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Abstract
Cellular senescence is associated with the accumulation of senescent cells that enhance the production of bioactive molecules known as the senescence-associated secretory phenotype (SASP).
- Senescent cells exhibit stable cell cycle arrest and loss of proliferative capacity.
- Key features of senescent cells include increased levels of cell cycle inhibitors and activation of DNA damage responses.
- SASP components, such as pro-inflammatory cytokines and growth factors, are secreted by senescent cells and can disrupt bone homeostasis.
- The accumulation of senescent cells during aging is linked to accelerated skeletal aging and osteoporosis.
- SASP is identified as a potential therapeutic target for age-related bone metabolic disorders, although its regulatory mechanisms in bone tissue cells are not fully understood.
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