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Mitochondrial metabolism and epigenetic crosstalk drive SASP

Research Cellular Senescence

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TL;DR - Mitochondrial acetyl-CoA drives inflammatory SASP activity through epigenetic changes in senescent cells. Targeting this metabolic pathway could help delay age-related functional decline.

Acetyl-CoA promotes histone acetylation and chromatin accessibility at inflammatory gene loci.
Inhibiting mitochondrial transporter SLC25A1 attenuates these effects.
The findings link mitochondrial metabolism, epigenetic regulation, and cellular senescence.

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Mitochondrial metabolism and epigenetic crosstalk drive SASP

Nature Hélène Martini, Jodie Birch, Francisco D. M. Marques, Stella Victorelli, Anthony B. Lagnado, Nicholas Pirius, Ana Catarina Franco, Gung Lee, Yeaeun Han, Jennifer L. Rowsey, Wazim Mohammed Ismail, Amelia Mazzone, Tianna M. Espe, Taro Hitosugi, Ya Li, Alexander M. Washington, Aaron Havas, Rabi Murad, Xue Lei, Rebecca A. Porritt, Oliver D. K. Maddocks, Jair Machado Espindola-Netto, Dominik Saul, Sundeep Khosla, Diana Jurk, Enis Kostallari, Alexandre Gaspar-Maia, Peter D. Adams, João F. Passos 2026-07-29 doi:10.1038/s41586-026-10791-2

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Providers: Hugging Face · N/A OpenAlex · Citations 1 Publisher · N/A Semantic Scholar · N/A X · N/A Fetched 2026-08-28 14:33:03.794428 UTC

TL;DR - Mitochondrial acetyl-CoA drives inflammatory SASP activity through epigenetic changes in senescent cells. Targeting this metabolic pathway could help delay age-related functional decline.

Acetyl-CoA promotes histone acetylation and chromatin accessibility at inflammatory gene loci.
Inhibiting mitochondrial transporter SLC25A1 attenuates these effects.
The findings link mitochondrial metabolism, epigenetic regulation, and cellular senescence.

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