| Literature DB >> 35102134 |
Zunpeng Liu1,2,3, Wei Li4,5, Lingling Geng4,5, Liang Sun6,7, Qiaoran Wang3,8,9, Yang Yu10, Pengze Yan3,11, Chuqian Liang3,11, Jie Ren2,3,8,9, Moshi Song2,3,11, Qian Zhao4,5, Jinghui Lei4,5, Yusheng Cai2,11,12, Jiaming Li3,8,9, Kaowen Yan2,11,12, Zeming Wu2,11,12, Qun Chu1,2,12, Jingyi Li2,11,12, Si Wang4,5, Chunyi Li13, Jing-Dong J Han14, Reyna Hernandez-Benitez15, Ng Shyh-Chang1,2,3, Juan Carlos Izpisua Belmonte15, Weiqi Zhang16,17,18,19, Jing Qu20,21,22,23, Guang-Hui Liu24,25,26,27,28,29.
Abstract
Regenerative capacity declines throughout evolution and with age. In this study, we asked whether metabolic programs underlying regenerative capability might be conserved across species, and if so, whether such metabolic drivers might be harnessed to promote tissue repair. To this end, we conducted metabolomic analyses in two vertebrate organ regeneration models: the axolotl limb blastema and antler stem cells. To further reveal why young individuals have higher regenerative capacity than the elderly, we also constructed metabolic profiles for primate juvenile and aged tissues, as well as young and aged human stem cells. In joint analyses, we uncovered that active pyrimidine metabolism and fatty acid metabolism correlated with higher regenerative capacity. Furthermore, we identified a set of regeneration-related metabolite effectors conserved across species. One such metabolite is uridine, a pyrimidine nucleoside, which can rejuvenate aged human stem cells and promote regeneration of various tissues in vivo. These observations will open new avenues for metabolic intervention in tissue repair and regeneration.Entities:
Year: 2022 PMID： 35102134 PMCID： PMC8803930 DOI： 10.1038/s41421-021-00361-3
Source DB: PubMed Journal: Cell Discov ISSN： 2056-5968 Impact factor: 38.079