What is the Origin of SASP?

The term emerged from cellular biology and gerontology research in the early 2000s, building upon the initial discovery of cellular senescence by Leonard Hayflick in the 1960s. The identification of the specific secretome—the collection of secreted molecules—that accompanies senescence provided a mechanistic link between non-dividing cells and systemic aging phenotypes. This discovery fundamentally changed the understanding of how aging progresses at the cellular level.

What is the Mechanism of SASP?

The activation of SASP is driven by DNA damage, telomere shortening, or oncogenic stress, which leads to the activation of transcription factors like NF-κB and C/EBPβ. These factors then induce the expression of genes encoding the various SASP components. The secreted molecules then act in an autocrine manner to reinforce the senescence arrest and in a paracrine manner to spread inflammation, recruit immune cells, and degrade the extracellular matrix in surrounding tissues. This self-perpetuating cycle of inflammation and damage is a core driver of biological aging.

SASP

Meaning

SASP is the acronym for the Senescence-Associated Secretory Phenotype, a complex, pro-inflammatory program activated in senescent cells—cells that have ceased dividing but remain metabolically active. This phenotype is characterized by the secretion of a potent mixture of pro-inflammatory cytokines, chemokines, growth factors, and proteases into the local tissue microenvironment. Clinically, the chronic presence of SASP-expressing cells is a major contributor to systemic “inflammaging,” tissue dysfunction, and the progression of numerous age-related pathologies, making its clearance a key target in longevity medicine.