What is the Origin of SASP Inhibition?

The concept is a direct product of molecular gerontology and cellular senescence research, which identified SASP as a key driver of age-related inflammation, or "inflammaging." The clinical utility of inhibition emerged from studies showing that removing or silencing senescent cells can improve organ function and delay age-related diseases. This strategy provides a targeted approach to managing the cumulative cellular damage of aging.

What is the Mechanism of SASP Inhibition?

SASP inhibition is achieved by using senomorphic agents that modulate the transcriptional pathways responsible for producing the inflammatory secretome. These agents target signaling pathways like NF-κB or mTOR, which are often hyperactive in senescent cells. By downregulating the secretion of these damaging factors, the intervention reduces chronic systemic inflammation and allows neighboring healthy cells to function without toxic interference.

SASP Inhibition

Meaning

SASP Inhibition refers to the therapeutic strategy of blocking or reducing the effects of the Senescence-Associated Secretory Phenotype (SASP), a detrimental set of pro-inflammatory molecules released by senescent, or “zombie,” cells. Senescent cells cease dividing but remain metabolically active, secreting cytokines, chemokines, and proteases that damage surrounding healthy tissue and accelerate aging. Inhibiting this secretion is a core mechanism of senolytic and senomorphic interventions, aiming to halt the spread of cellular dysfunction. This process is crucial for improving tissue microenvironments and extending healthspan.