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. 2018 Dec 21;8:18024. doi: 10.1038/s41598-018-36626-3

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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 working model that TLR4 disruption ameliorates adipose tissue remodeling during cancer cachexia syndrome. Cancer-induced cachexia is characterized by systemic inflammation, body weight loss and AT remodeling. We show that TLR4 disruption (knockout model of TLR4 and pharmacological inhibition by ATOR treatment) ameliorates AT remodeling, in particular, preservation of adipocyte atrophy and attenuation of browning phenotype in scAT, as well as inflammatory responses during cancer cachexia syndrome. Additionally, TLR4 disruption was effective in prolonging the survival and reducing tumor mass growth. Therefore, these data suggest that TLR4 plays an important role during cachexia development. Here, we suggested a new potential therapeutic target for cancer cachexia syndrome. Parts of the figure were drawn using images from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 3.0 Unported License (https://smart.servier.com/).