Scientists find how senescent cells fuel age-related inflammation

September 13, 2026 at 05:00 AM1 min

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Researchers at Sanford Burnham Prebys and Mayo Clinic identified a mitochondrial mechanism that drives chronic inflammation in aging cells. The findings, published in Nature, show that senescent cells produce excess acetyl-CoA, which alters DNA packaging to activate inflammatory genes. Interfering with this process reduced inflammation and improved health in aging mice.

Key Facts

The study was published in Nature by researchers from Sanford Burnham Prebys Medical Discovery Institute and Mayo Clinic.
Senescent cells remain metabolically active and secrete inflammatory molecules, a state known as the senescence-associated secretory phenotype (SASP).
Mitochondria in senescent cells produce increased amounts of acetyl-CoA, which interacts with histones to promote SASP gene expression.
Interfering with the identified pathway reduced inflammation and supported healthier aging in mice.

Senescent Cell Inflammation

As people age, increasing numbers of cells enter a state known as senescence, where they stop dividing but remain alive and metabolically active. These senescent cells activate an inflammatory program called the senescence-associated secretory phenotype (SASP), which is linked to widespread age-related inflammation and chronic diseases. Peter Adams, PhD, co-corresponding author at Sanford Burnham Prebys, noted that senescent cells are not completely inert and secrete inflammatory molecules.

Mitochondrial Mechanism

Researchers led by João Passos, PhD, at Mayo Clinic found that mitochondria in senescent cells produce increased amounts of acetyl-CoA, a key metabolic molecule. Acetyl-CoA interacts with histones, the proteins around which DNA is wrapped, altering how DNA is stored to promote SASP-related gene expression. The team identified a convergence of at least two mitochondrial-related biological pathways that drive the inflammatory phenotype.

Therapeutic Potential

Interfering with part of the identified process reduced inflammation and supported healthier aging in mice. The study suggests that targeting mitochondrial acetyl-CoA production or its effects on histones could be a strategy to mitigate age-related inflammation.