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. 2018 May 3;8:6997. doi: 10.1038/s41598-018-25485-7

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© The Author(s) 2018

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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The suggested mechanism by which CPT1C increases cell survival in hMSCs under glucose starvation. hMSCs show reduced autophagic flux under glucose starvation. CPT1C overexpression increases autophagy and LD number in glucose-deficient conditions, which results in increased fatty acid availability for mitochondrial β-oxidation, and consequently, higher levels of ATP and longer cell survival compared to control cells.