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. 2024 Jan 18;22:73. doi: 10.1186/s12967-023-04845-6

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© The Author(s) 2024

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 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. 1 — A The mitochondrial dynamic paradigm. Mitochondria undergo dynamic changes in shape by the two opposite processes of fission and fusion. Mitochondrial fusion of the outer membrane is mediated by MFNs. Fusion of the inner mitochondrial membrane is regulated by OPA1. Mitochondrial fission requires DRP1 phosphorylation and recruitment. In HCC, impaired mitochondrial dynamic equilibrium induces tumor proliferation, drug resistance, metastasis, and stem properties. B Flow chart of construction and validation of a prognostic signature for LIHC. MFNs mitofusins, OPA1 optic atrophy 1, DRP1 dynamin-related protein 1, HCC hepatocellular carcinoma. LIHC liver hepatocellular carcinoma