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. 2023 Apr 3;8:144. doi: 10.1038/s41392-023-01351-5

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© The Author(s) 2023

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Model of tG026 mechanism in liver injury. Loss of NSun2 can ameliorate liver injury produced by CCl₄ injection. Mechanistically, the loss of NSun2 reduces m⁵U and m⁵C modifications. Hence, the tRNAs become unstable and produce tsRNAs, particularly tRF-1s. Through further screening experiments, tG026 was found to inhibit the association between TSR1 and 18S rRNA by interacting with TSR1, thereby reducing global protein synthesis and alleviating liver injury