Senescent cell signaling
Senescence-associated secretory phenotype (SASP)↓
Also searched as Senescence-associated secretory phenotype (SASP).
The mix of inflammatory signals that senescent cells secrete. It is how a small number of worn-out cells make trouble far beyond themselves, spreading inflammation through the surrounding tissue — though the same signals also flag those cells for immune clearance.
In depth
The senescence-associated secretory phenotype — what a senescent cell says to its neighbors. Self-reinforcing: sasp drives inflammaging, and inflammaging drives more sasp. An arrow encodes one pass of a loop.
What drives it
Clears worn-out cells increases it.
Senescent cells display a secretory phenotype involving factors that reinforce the arrest, alter the microenvironment, and trigger immune surveillance. doi 10.1016/j.cellsig.2011.12.006 · PMID 21979375 · PMC7767554
Calms inflammation increases it.
NF-kB acts as a master regulator of the SASP, influencing the expression of more genes than RB and p53 combined. doi 10.1016/j.cellsig.2011.12.006 · PMID 21979375 · PMC7767554
Growth restraint increases it.
mTOR drives the translation of SASP components. doi 10.1016/j.cellsig.2011.12.006 · PMID 21979375 · PMC7767554
DNA integrity increases it.
Genotoxic insults initiate the senescent phenotype and the persistent DNA-damage response sustains the secretory program. doi 10.1016/j.cellsig.2011.12.006 · PMID 21979375 · PMC7767554
What it drives
It increases Calms inflammation.
NF-kB acts as a master regulator of the SASP, influencing the expression of more genes than RB and p53 combined. doi 10.1016/j.cellsig.2011.12.006 · PMID 21979375 · PMC7767554
It increases Calms body-wide inflammation.
Senescent cells accumulate over the course of normal aging, and their secretory phenotype is a crucial driver of chronic inflammation and aging phenotypes. doi 10.1016/j.cellsig.2011.12.006 · PMID 21979375 · PMC7767554
It increases Immune support.
NF-kB suppression causes escape from immune recognition by natural killer cells; BRD4 inhibition blunts the SASP and leads to reduced NK-cell-mediated immunosurveillance of senescent cells. doi 10.1016/j.cellsig.2011.12.006 · PMID 21979375 · PMC7767554
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.