University of Rochester researchers have found that a protein long associated with chronic inflammation and aging may also play an important protective role, complicating efforts to target it in therapies for age-related disease.
The protein, known as cGAS, can detect DNA that appears in the wrong place inside a cell and trigger an inflammatory response. Researchers have been studying the protein because persistent inflammation can contribute to cell damage and diseases associated with aging, including cancer.
Scientists had believed that suppressing cGAS could help slow aging by reducing inflammation. But a new study published in Nature Aging found the opposite effect in mice: removing cGAS caused them to age faster.
The findings suggest the protein may have both harmful and beneficial roles, depending on the biological context.
Vera Gorbunova, Ph.D., the Doris Johns Cherry Professor in the University of Rochester Department of Biology and a member of Wilmot Cancer Institute, said cGAS has become an important focus of research because of its connection to inflammation and immune activity.
The immune system is closely tied to cancer development and progression, making cGAS of particular interest to researchers studying both aging and cancer.
The new results challenge the assumption that reducing cGAS activity would necessarily produce anti-aging benefits. Instead, researchers said a better understanding of the protein’s opposing functions will be needed before therapies are designed to target it.
The work was conducted by Gorbunova’s laboratory with co-investigator Andrei Seluanov, Ph.D., a Dean’s professor of biology at the University of Rochester.
The study adds to broader research examining how inflammation, immune responses and cellular damage interact during aging and could influence future approaches to treating diseases linked to those processes.
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