由Sanford Burnham Prebys医学发现研究所和Mayo Clinic等机构组成的研究团队发现了衰老细胞驱动慢性炎症的分子机制。1这项发表于《自然》杂志的研究表明，功能障碍的线粒体在这一过程中起到关键作用。1
衰老细胞进入衰老状态后停止分裂，但仍保持代谢活跃。1研究发现，这些细胞的线粒体会产生过量乙酰辅酶A，该物质与组蛋白相互作用，导致DNA包装变松散，使炎症基因更容易被激活。1与此同时，受损线粒体泄漏的DNA和RNA被免疫系统识别为危险信号，进一步激活相关转录因子，引发衰老相关分泌表型（SASP）基因的表达。1
科研人员测试了CTPI-2药物以阻断乙酰辅酶A的生成。1在小鼠实验中，该药物治疗减少了SASP基因的可访问性，有效缓解了多个组织的炎症，改善了组织功能和健康寿命。1
Researchers have identified the mechanism by which senescent cells—often called "zombie" cells—fuel chronic inflammation associated with aging.1 The study, published in Nature on September 13, 2026, was conducted by teams at Sanford Burnham Prebys Medical Discovery Institute and Mayo Clinic, led by Dr. João Passos.1
Senescent cells enter a state where they stop dividing but remain metabolically active.1 The research reveals that dysfunctional mitochondria within these cells produce excess acetyl-CoA, which interacts with histones to loosen DNA packaging and expose inflammatory genes.1 Simultaneously, damaged mitochondria leak DNA and RNA that the immune system recognizes as danger signals, activating transcription factors that switch on these inflammatory genes.1
The findings offer a potential therapeutic avenue: treatment with CTPI-2, a drug that blocks acetyl-CoA production, reduced the accessibility of senescence-associated secretory phenotype (SASP) genes.1 In mice, CTPI-2 treatment alleviated inflammation across multiple tissues, improved tissue function, and enhanced healthspan.1
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