University of Rochester researchers found that removing a protein associated with persistent inflammation caused mice to age faster, challenging expectations that blocking it could slow aging. The finding suggests the protein, known as cGAS, may have both harmful and protective roles.
cGAS detects DNA that appears in the wrong part of a cell and can trigger inflammation. Scientists have studied it because chronic inflammation can damage cells and contribute to age-related diseases, including cancer.
Researchers had believed that shutting down cGAS might reduce inflammation and slow the aging process. In the new work, published in the journal Nature Aging, mice without the protein instead aged more quickly.
Vera Gorbunova, the Doris Johns Cherry Professor in the University of Rochester's Department of Biology and a member of Wilmot Cancer Institute, said cGAS has become a major focus of research.
The immune system is closely connected to cancer activity, making the protein's signaling role relevant to efforts to understand inflammation and disease. The unexpected result indicates that therapies designed to inhibit cGAS may need to account for its opposing effects.
Gorbunova's laboratory conducted the work with co-investigator Andrei Seluanov, a Dean's Professor of Biology at the university. The researchers said a clearer understanding of cGAS could influence future strategies aimed at reducing age-related inflammation.
The study was conducted in mice, and the source did not report results from human clinical trials.
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