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. 2023 Mar 2;14:1199. doi: 10.1038/s41467-023-36817-1

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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. 8 — Scheme illustrating the role of MYTHO in skeletal muscle homeostasis. Acute MYTHO depletion protects from atrophy in different catabolic conditions (starvation, cancer cachexia, denervation, and sepsis). Prolonged MYTHO depletion in skeletal muscle blunts autophagic flux and triggers a sustained hyperactivation of growth signaling causing a myopathological phenotype, characterized by pathological hypertrophy, myofiber degeneration, impaired force generation, and major ultrastructural abnormalities. KD Knockdown. Created with BioRender.com.