GEO series

Mitochondrial metabolism and epigenetic crosstalk drive the SASP (Multiome)

GSE324238 Mus musculus Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2026/05/19 Platform GPL21103

Summary

Senescent cells drive age-related tissue dysfunction largely through the persistent activation of the senescence-associated secretory phenotype (SASP). Here, we identify key mitochondrial metabolic pathways, including the mitochondrial citrate carrier (SLC25A1) and ATP-citrate lyase (ACLY), as critical regulators of the SASP. These pathways fuel histone acetylation at SASP gene loci, promoting their expression. Targeted inhibition of SLC25A1 or ACLY suppresses SASP expression without affecting cell cycle arrest, underscoring their potential as selective therapeutic targets for mitigating age-related inflammation. Furthermore, pharmacological inhibition of SLC25A1 reduces systemic inflammation and extends healthspan in aged mice. Our findings suggest that disrupting metabolic reprogramming in senescent cells offers a promising strategy to ameliorate aging-associated pathologies.

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Also filed as BioProject PRJNA1434289 and SRA study SRP682180. Searching any of these in the dataset finder brings you back here.

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