Senescence-associated secretory phenotype (SASP)

The senescence-associated secretory phenotype (SASP) is a dynamic and highly variable cellular program in which senescent cells secrete a broad array of bioactive molecules, including proinflammatory cytokines, chemokines, growth factors, and proteases, into their microenvironment[1][7][10]. These factors mediate widespread biological effects, from promoting wound healing and tissue remodeling to driving chronic inflammation, immune cell recruitment, and both suppression and progression of tumorigenesis, depending on context[2][4][6][8]. SASP composition is tissue- and stimulus-dependent, and key secreted molecules—such as IL-6 and IL-8—are considered hallmark features. SASP is not a single molecule or canonical target, but a broad collective phenotype that contributes to aging and age-associated diseases by modulating both local tissue environments and systemic biology[1][2][3][7]. SASP is not a single molecular target, enzyme, transporter, receptor, or protein but rather a complex secretory phenotype (i.e., a functional program or signature of many molecules) produced by senescent cells[1][2][7]. As such, it is conceptually important in disease biology and drug development strategy, but it does not fit the definition of a canonical molecular target for drug binding or inhibition[1][6][7]. Instead, therapies commonly aim to modulate SASP as a whole (senomorphics) or remove the cells producing it (senolytics)[2]. Some individual components of SASP (such as IL-6) are themselves canonical drug targets.

Other names

Senescence-messaging secretomeSMS

None specific; senolytics clear senescent cells to reduce SASP, senomorphics suppress the secretion of SASP factors