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. 2022 Feb 22;12:2996. doi: 10.1038/s41598-022-06542-8

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© The Author(s) 2022

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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Mechanisms of steatohepatitis-related cardiomyopathy and the effects of pemafibrate. Cholesterol absorbed from the NASH diet is first taken up by the liver. Some of the free cholesterol in the liver becomes cholesterol crystals, which are taken up by macrophages and hepatocytes and lead to the production of IL-1β. In addition, macrophages produce Ccl5, which activates stellate cells and causes liver fibrosis. Free cholesterol in VLDL and LDL is taken up into the myocardium, where it activates macrophages and inflammasomes of myocardial cells, induces IL-1β production, and causes LV hypertrophy and dysfunction. Furthermore, ROS generated by an increase in free cholesterol are also considered to be involved in cardiac dysfunction. Pemafibrate reduces the level of free cholesterol in the liver and inhibits the production of cholesterol crystals, thereby suppressing the activity of inflammasomes and inhibiting the development of steatohepatitis. As a result, serum VLDL, LDL, and TNF-α were reduced and HDL was increased. Free cholesterol in the myocardium was reduced and inhibited myocardial damage via suppression of myocardial inflammasome activity.