An enzyme called SETD8 appears to play a critical role in cellular senescence onset
Senescent cells may have stopped dividing, but they continue to remain active - churning out a specific cocktail of factors that increases inflammation and breaks down tissue among other things. Stopping cells becoming senescent in the first place, or removing them once they arise, has been shown to rejuvenate and protect animals as they age.
SETD8 and senescence
Researchers studying senescence mechanisms at Kumamoto University in Japan have now uncovered an enzyme that appears to regulate cellular senescence. By screening cultured human fibroblast cells they isolated an enzyme called SETD8 methyltransferase. SETD8 is known to methylate histone H4 lysine 20 (H4K20), and play a role in cell proliferation. Through this new research the team found reduced levels of SETD8 were strongly correlated with senescence.
When they tested this by knocking down SETD8 and inhibiting it, cells displayed typically senescent features. More specifically, reduced SETD8 promoted genes involved with protein synthesis and growth arrest, just as in normal senescent cells. It also activated mitochondria, which again is characteristic to senescent cells. With further research, it may prove an additional drug target to modulate and prevent senescence from occurring.
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