斯坦福医学研究团队发现，在免疫细胞上阻断名为EP2的单一受体可能是延缓衰老的关键。1 研究人员在小鼠实验中发现，删除组织驻留巨噬细胞上的EP2基因使老年小鼠在多个器官中保持了年轻特征，包括更强的肌肉、更少的脂肪、更好的认知功能和更低的炎症水平。1 这一发现发表在《科学》杂志2026年第393卷第6808期上。1
在生物学机制上，阻断EP2受体能帮助清除衰老的中性粒细胞，从而减少全身炎症。1 研究对比了年长小鼠（23-25个月，相当于人类60-70岁）与删除EP2基因的老年小鼠，发现血液中71种蛋白质水平发生了显著变化，其中59种在缺乏EP2的小鼠中保持在年轻水平。1 删除EP2后，老年小鼠每天需清除的中性粒细胞数量约为100亿个。1
研究团队还验证了药物干预的可行性，一种实验药物在22个月大的小鼠中使用2个月，使中性粒细胞水平接近年轻小鼠水平。1 资深作者Katrin Andreasson医学博士指出："衰老中性粒细胞正在杀死我们的组织。清除这些细胞对防止慢性炎症至关重要。"1 目前尚无获批药物能选择性关闭EP2活性。1
Stanford Medical researchers have identified a potential therapeutic target in the aging process: blocking a single receptor called EP2 on immune cells can help clear senescent neutrophils and reduce systemic inflammation.1 In experiments with mice, deleting the EP2 gene in tissue-resident macrophages enabled older mice to maintain youthful characteristics across multiple organs, including stronger muscles, less fat, improved cognitive function, and lower inflammatory levels.1 The study, published in Science in 2026 (Volume 393, Issue 6808), compared aged mice aged 23–25 months—equivalent to humans in their 60s to 70s—with those lacking EP2 and found that 59 of 71 blood proteins that had changed significantly with age remained at youthful levels in the EP2-deficient animals.1
In the EP2-deficient mice, approximately 10 billion senescent neutrophils required clearance daily.1 When an experimental drug was administered to 22-month-old mice for two months, neutrophil levels dropped to near those of young mice.1 The research team was led by Dr. Jessy Tan, a neurology lecturer, with Dr. Katrin Andreasson as the senior author.1 According to Andreasson, "Aging neutrophils are killing our tissues. Clearing these cells is critical to preventing chronic inflammation."1 The researchers noted that currently no approved drugs can selectively shut down EP2 activity.1
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