Inhibiting the STING protein in aged mice leads to decreased inflammation and improved memory and physical function, highlighting a promising approach to mitigating aging-related challenges.
As we age, our bodies undergo various changes that can impact our overall health and make us more susceptible to diseases. One common factor in the aging process is low-grade inflammation, which contributes to age-related decline and impairment. However, the precise pathways responsible for this inflammation and their impact on natural aging have remained elusive until now.
The Role of cGAS/STING in Aging
A new study led by Andrea Ablasser at EPFL now shows that a molecular signaling pathway called cGAS/STING, plays a critical role in driving chronic inflammation and functional decline during aging. By blocking the STING protein, the researchers were able to suppress inflammatory responses in senescent cells and tissues, leading to improvements in tissue function.
cGAS/STING is a molecular signaling pathway that detects the presence of
Link Between cGAS/STING and Cellular Senescence
Previous work by Ablasser and her colleagues has linked cGAS/STING to a number of biological processes, including cellular senescence, a hallmark of aging. Based on this, the researchers investigated whether it might underlie maladapted immune responses during aging.
The research found that activating the STING protein triggers specific patterns of gene activity in microglia, the brain’s first line of defense immune cells. These gene-activation patterns matched those arising in microglia in distinct neurodegenerative conditions, such as Alzheimer`s disease and aging.
“In search for a mechanism that would engage the cGAS-STING pathway in aging, we considered aberrant mitochondrial DNA DOI: 10.1038/s41586-023-06373-1
Funding: Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung, Horizon 2020 Framework Programme, Dr. Josef Steiner Krebsstiftung, Krebsliga Schweiz