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. 2022 Jan 10;8:824481. doi: 10.3389/fcvm.2021.824481

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Copyright © 2022 Hoebinger, Rajcic and Hendrikx.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Genetics, sedentary lifestyle and/or unhealthy nutrition causes systemic dyslipidemia characterized by increased LDL levels. Due to oxidative stress and ROS production, oxidation-specific epitopes present on oxidized lipids, dying cells, and microvesicles accumulate. Receptor-mediated recognition and uptake of oxidized lipoproteins by macrophages in the steatotic liver and atherosclerotic plaque results in a foamy appearance, lysosomal dysfunction, and cholesterol crystals formation, causing pro-inflammatory signaling and thereby enhancing disease progression.