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. 2024 Jan 16;14:1438. doi: 10.1038/s41598-024-51996-7

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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/.

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Ketosis impacts AAA expansion and risk of rupture. AAA expansion and risk rupture is influenced by CCR2, which in turn recruits CD68+ pro-inflammatory macrophages, and also leads to cytokine release, and MMP activation. Vascular smooth muscle cells (VSMCs) production of TIMP1 can complex with MMP9 to help balance out the rate of MMP-medicated ECM degradation. Decreased TIMP1/MMP9 complex can lead to higher ECM degradation and AAA expansion. CCR2-mediated release of TNFα, RANTES, IL-10, IL-17A, and IFNγ can further compound AAA tissue stability, and inhibition of TGFβ can progress AAA instability, which further escalates the risk of rupture. Ketosis inhibits inflammation and ECM degradation thereby stabilizes AAA tissue and reduces the risk of rupture. Figure was made using BioRender.com.