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Mitochondrial metabolism drives inflammatory ageing via epigenetic crosstalk
In senescent cells, mitochondria-derived acetyl-CoA promotes histone acetylation and increases chromatin accessibility at inflammatory gene sites, fuelling the senescence-associated secretory phenotype (SASP). Inhibiting the transporter SLC25A1 reduces these effects. The findings identify mitochondrial metabolism as a potential therapeutic target for slowing age-related functional decline.
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