继续追寻长生不老药，nature最新发现

2024年7月，NATURE上线一篇论文“Inhibition of IL-ll signalling extends mammalian health span and lifespan”今天，作者是来自杜克-新加坡国立大学医学院的Stuart A. Cook和Anissa A. Widjaja领衔的研究团队。

这个研究发现，促炎细胞因子IL-11在哺乳动物健康和寿命中发挥重要的调控作用。IL-11的水平会随年龄逐渐增加。采用基因敲除或者药物干扰IL-11，可显著提升小鼠寿命，同时对年龄增加导致的多器官组织变化有显著改善作用。

我的评价：NATURE这个论文啊，也是提出一个观点，真的有延长寿命的长生不老药，可惜，我比较有疑问的是，人体进化这么多年，是不是真的有某些特别坏的基因，它真的一无是处。

下附论文摘要：

For healthspan and lifespan, ERK, AMPK and mTORC1 represent critical pathways and inflammation is a centrally important hallmark1-7. Here we examined whether IL-11, a pro-inflammatory cytokine of the IL-6 family, has a negative effect on age-associated disease and lifespan. As mice age, IL-11 is upregulated across cell types and tissues to regulate an ERK-AMPK-mTORC1 axis to modulate cellular, tissue- and organismal-level ageing pathologies. Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age. Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes. In lifespan studies, genetic deletion of Il11 extended the lives of mice of both sexes, by 24.9% on average. Treatment with anti-IL-11 from 75 weeks of age until death extends the median lifespan of male mice by 22.5% and of female mice by 25%. Together, these results demonstrate a role for the pro-inflammatory factor IL-11 in mammalian healthspan and lifespan. We suggest that anti-IL-11 therapy, which is currently in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people.