Nature aging · 2026
Single-nucleus interrogation of primate small intestinal aging reveals NCoR1 decline as a conserved feature that is reversed by metformin.
СтатьяНазвание и аннотация: Перевод в очереди
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Li Jingyi, Lu Xiaoyong, Tong Tianhong, Zhou Xin, Zhang Baohu, Sun Xiaoyan, Zhao Bing, Xu Gang, Yang Jinjiang, Fan Yanling, Hu Jianli, Yan Haoteng, Ji Zhejun, Li Mingheng, Che Shanshan, Yang Yuanhan, Ding Yingjie, Wang Qiaoran, Sun Shuhui, Ma Shuai, Wang Si, Izpisua Belmonte Juan Carlos, Qu Jing, Zhang Weiqi, Liu Guang-Hui
Аннотация
How the small intestine ages at the cellular and molecular level has been unclear. Here we profile single nuclei from young and aged primate small intestine and find that aging brings barrier dysfunction, chronic inflammation and a shift in stem cell differentiation away from absorptive cells toward secretory cells. Through integrative multimodal analysis, we identify the transcriptional corepressor NCoR1 as a key player whose decline is conserved in the aging human gut. In human intestinal epithelial cells and organoids, knocking down NCOR1 recapitulates aging phenotypes including senescence, disrupted junctions and lineage imbalance, whereas overexpressing NCoR1 alleviates them. Metformin-a geroprotective drug-restores NCoR1 levels and delays intestinal aging in nonhuman primates. Our work points to NCoR1 as a central regulator of small intestinal aging and suggests a pharmacologically actionable strategy to counter age-related intestinal decline.