Core Viewpoint - The article discusses a recent study revealing the mechanism by which chromatin fragments are released from the nucleus during aging, highlighting the potential of targeting this process to inhibit age-related inflammation [3][6]. Group 1: Research Findings - The study published by a team from Harvard Medical School/Massachusetts General Hospital identifies "Nuclear Egress" as a mechanism for the export of chromatin fragments from the nucleus, which is crucial for understanding chronic inflammation in aging [3][6]. - The research demonstrates that inhibiting key nuclear egress proteins, such as the ESCRT-III complex, can prevent chromatin fragments from activating the cGAS-STING pathway, thereby reducing age-related inflammation [6]. - Metformin treatment was shown to significantly lower ALIX expression in intestinal tissues of aged mice, leading to decreased levels of chromatin fragments and reduced cGAS-mediated inflammatory responses [6]. Group 2: Implications for Treatment - The findings suggest a novel therapeutic strategy targeting the nuclear release of chromatin fragments to mitigate age-related inflammation, linking metabolic interventions with inflammatory responses [6]. - The study indicates that both glucose restriction and metformin can inhibit the formation of chromatin fragments through AMPK-dependent phosphorylation and autophagic degradation pathways [6].