Cellular senescence and the senescence-associated secretory phenotype (SASP) contribute to age-related musculoskeletal decline by promoting chronic inflammation, impairing muscle regeneration, and accelerating bone resorption, as demonstrated in animal models where clearance of senescent cells improved muscle strength and bone density.

Old cells stop dividing and release harmful chemicals that trigger inflammation, damage muscle and bone tissue, block muscle repair, and weaken bones. These chemicals also make nearby cells become old and dysfunctional, spreading the damage. The inflammation reduces blood flow to muscles, impairs nerve signals to muscles, and causes pain that limits movement. When these old cells are removed, inflammation drops, muscles get stronger, and bones become denser.