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. 2023 Jan 20;21:36. doi: 10.1186/s12967-023-03885-2

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Mechanism and function of MOTS-c. Short open reading frame on 12S rRNA of mitochondrial DNA transcribes mRNA in mitochondria. Subsequently, the mRNA translocates to the cytoplasm to translate MTOS-c. MOTS-c is triggered to translocate into the nucleus by stress, exercise and aging through the AMPK/PGC-1α-dependent pathway, thereby regulating the expression of genes with antioxidant response elements (ARE) and stress adaptation-related. MOTS-c can mainly regulate the folate cycle and de novo purine biosynthesis pathway, leading to an increase in AICAR, which phosphorylates and activates AMPK. AMPK can regulate energy homeostasis and produce anti-inflammatory effects by activating SIRT1 and PGC-1α (Phosphorylation and deacetylation). In addition, AMPK can promote nuclear translocation of MOTS-c, forming a feedback loop