Nature, Published online: 29 July 2026; doi:10.1038/s41586-026-10791-2

In senescent cells, mitochondria-derived acetyl-CoA promotes histone acetylation and increases chromatin accessibility at inflammatory gene loci. Inhibition of SLC25A1 attenuates these effects, underscoring the therapeutic potential of targeting mitochondrial metabolism and its epigenetic crosstalk to delay age-related functional decline.