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. 2017 Jul 26;7:6618. doi: 10.1038/s41598-017-07011-3

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© The Author(s) 2017

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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Schematic presentation of the proposed model: Role of protein farnesylation in burn-induced metabolic derangements. Our data indicate that protein farnesylation causes and/or exacerbates activation of the HIF-1α pathway and mTORC1, mitochondrial dysfunction, and ER stress, all of which contribute in concert to burn-induced muscle metabolic derangements, including insulin resistance and increases in lactate production and protein breakdown. Farnesyltransferase (FTase) inhibitor (FTI) prevents burn-induced metabolic derangements by inhibiting or mitigating the impact of burn injury on HIF-1α, mTORC1, mitochondria, and ER stress in mouse skeletal muscle.