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In contrast, embryonic and foetal progenitors typically possess heightened proliferative capacities and manifest a more robust regenerative response upon injury and transplantation, despite undergoing many rounds of mitosis. How embryonic and foetal progenitors delay senescence and maintain their proliferative and differentiation capacities after numerous rounds of mitosis, remains unknown. It is also unclear if defined embryonic factors can rejuvenate adult progenitors to confer extended proliferative and differentiation capacities, without reprogramming their lineage\u2010specific fates or inducing oncogenic transformation. Here, we report that a minimal combination of LIN28A, TERT, and sh\u2010p53 (LTS), all of which are tightly regulated and play important roles during embryonic development, can delay senescence in adult muscle progenitors. LTS muscle progenitors showed an extended proliferative capacity, maintained a normal karyotype, underwent myogenesis normally, and did not manifest tumorigenesis nor aberrations in lineage differentiation, even in late passages. LTS treatment promoted self\u2010renewal and rescued the pro\u2010senescence phenotype of aged cachexia patients' muscle progenitors, and promoted their engraftment for skeletal muscle regeneration in vivo. When we examined the mechanistic basis for LIN28A's role in the LTS minimum combo, <jats:italic>let\u20107<\/jats:italic> microRNA suppression could not fully explain how LIN28A promoted muscle progenitor self\u2010renewal. Instead, LIN28A was promoting the translation of oxidative phosphorylation mRNAs in adult muscle progenitors to optimize mitochondrial reactive oxygen species (mtROS) and mitohormetic signalling. Optimized mtROS induced a variety of mitohormetic stress responses, including the hypoxic response for metabolic damage, the unfolded protein response for protein damage, and the p53 response for DNA damage. Perturbation of mtROS levels specifically abrogated the LIN28A\u2010driven hypoxic response in Hypoxia Inducible Factor\u20101\u03b1 (HIF1\u03b1) and glycolysis, and thus LTS progenitor self\u2010renewal, without affecting normal or TS progenitors. Our findings connect embryonically regulated factors to mitohormesis and progenitor rejuvenation, with implications for ageing\u2010related muscle degeneration.<\/jats:p>","DOI":"10.1111\/cpr.13459","type":"journal-article","created":{"date-parts":[[2023,5,13]],"date-time":"2023-05-13T06:40:20Z","timestamp":1683960020000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Adult progenitor rejuvenation with embryonic factors"],"prefix":"10.1111","volume":"56","author":[{"given":"Peng","family":"Wang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Reproductive Biology, Institute of Zoology Chinese Academy of Sciences  Beijing China"},{"name":"Beijing Institute for Stem Cell and Regenerative Medicine Institute for Stem Cell and Regeneration, Chinese Academy of Sciences  Beijing China"},{"name":"University of Chinese Academy of Sciences  Beijing 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