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. 2023 Jan 24;14(1):57. doi: 10.1038/s41419-023-05599-1

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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. 3 — Downregulation of CPT1C favors cancer cell senescence, as demonstrated by the increased b-galactosidase marker, diminished telomere length, cell cycle arrest, and activation of the senescence-associated secretory phenotype. CPT1C downregulation, as revealed by lipidomic analysis, results in great lipid remodeling, including impaired expression of lipid metabolic genes, decreased cardiolipin levels, diminished phosphatidylcholine/phosphatidylethanolamine (PC/PE) ratio, increased levels of FAs, triacylglycerol, and sphingolipids, and lipid droplet accumulation. CPT1C downregulation impairs mitochondrial morphology, function (decreased mitochondrial respiration, decreased FAO, and altered electrochemical gradient) and biogenesis. All those changes result in decreased ATP levels and oxidative stress.