What is senescence?
Senescence is a state in which a cell stops dividing (permanent growth arrest) but remains alive and metabolically active. Senescent cells often secrete pro-inflammatory factors (the SASP) that damage neighboring cells and drive aging.
Key Concepts
- •SASP — Senescence-Associated Secretory Phenotype; cytokine/protease "cocktail"
- •Zombie cells — accumulate with age, driving chronic inflammation
- •Senolytics — compounds that selectively eliminate senescent cells
- •Apoptosis — programmed cell death; senolytics induce it in senescent cells
Why does Senescence matter?
Cellular senescence matters because it is one of the body's ways of stopping damaged cells from multiplying. When a cell has too much DNA damage or other stress, it can enter a permanent growth arrest instead of risking becoming cancerous.
The trade-off is that senescent cells often remain in tissues and release inflammatory signals. As people age, and as clearance by the immune system becomes less efficient, these cells accumulate. Research links this build-up to tissue aging, though how much it drives specific human diseases is still being worked out.
What affects Senescence?
Senescence is triggered mainly by cellular stress. Repeated cell division shortens telomeres, and damage from radiation, some chemotherapy, oxidative stress and oncogene activation can all push cells into this state.
How quickly senescent cells accumulate also depends on how well the immune system clears them, which tends to decline with age. Animal studies show that removing senescent cells can improve some age-related changes, but in humans evidence for senolytic drugs is still early. Claims that supplements reliably reduce senescence are not well supported.
In ONDA Life
The Senolytic High-Dosing article covers quercetin/fisetin and other senolytic protocols.