Gut microbial-derived phenylacetylglutamine accelerates host cellular senescence.

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Tác giả: Xiejiu Chen, Mengwei Fu, Yiqin Huang, Jianliang Jin, Yong Lin, Nan Liu, Tao Liu, Xueguang Liu, Miaomiao Pan, Chenglang Qian, Peng Qiao, Yifan Qu, Xingyu Rong, Meifang Shi, Ning Sun, Huijing Wang, Tongyao Wang, Yumei Wen, Yonglin Wu, Zhenming Xiao, Hao Yang, Hui Yang, Anaguli Yeerken, Dong Yu, Ming Zhang, Chao Zhao, Yufan Zheng

Ngôn ngữ: eng

Ký hiệu phân loại: 305.568 +Alienated and excluded classes

Thông tin xuất bản: United States : Nature aging , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 60417

Gut microbiota plays a crucial role in the host health in the aging process. However, the mechanisms for how gut microbiota triggers cellular senescence and the consequent impact on human aging remain enigmatic. Here we show that phenylacetylglutamine (PAGln), a metabolite linked to gut microbiota, drives host cellular senescence. Our findings indicate that the gut microbiota alters with age, which leads to increased production of phenylacetic acid (PAA) and its downstream metabolite PAGln in older individuals. The PAGln-induced senescent phenotype was verified in both cellular models and mouse models. Further experiments revealed that PAGln induces mitochondrial dysfunction and DNA damage via adrenoreceptor (ADR)-AMP-activated protein kinase (AMPK) signaling. Blockade of ADRs as well as senolytics therapy impede PAGln-induced cellular senescence in vivo, implying potential anti-aging therapies. This combined evidence reveals that PAGln, a naturally occurring metabolite of human gut microbiota, mechanistically accelerates host cellular senescence.
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