STING deficiency extends median lifespan and mitigates age-related liver pathology in mice
Abstract
The cGAS-STING pathway is a major driver of chronic inflammation. While acute STING inhibition can reduce neuroinflammation and tissue damage, its long-term impact on longevity remains unknown. Here, we demonstrate that genetic deletion of STING extends median lifespan in mice. This survival benefit is accompanied by a marked resistance to age-related hepatic decline. Our findings demonstrate that targeting STING is a promising therapeutic target to extend healthy lifespan.
The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.
Research summary
Genetic deletion of STING extends median lifespan and mitigates age-related liver pathology in mice. This paper is relevant because it identifies a specific molecular pathway (cGAS-STING) whose chronic activation drives inflammation and organ decline, and demonstrates that targeting this root cause of aging-related pathology can extend lifespan, rather than merely treating a specific age-related symptom.
Author of this paper? Send a correction.