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. 2023 Jan 25;22:12. doi: 10.1186/s12944-023-01777-4

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© The Author(s) 2023

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Schematic view of roles of chemerin in preeclampsia dyslipidemia. In preeclampsia condition, a high level of chemerin is released from trophoblasts in the placenta, inducing an inflammatory condition and further increasing the levels of placental lipids (TG, Chol, and phospholipids), lipid droplet accumulation, and the TCA cycle. Meanwhile, chemerin inhibits LDL uptake by reducing LDLR and SORT1 in trophoblasts, which leads to an increase in the release of lipids and the lipid-related protein (TG, Chol, phospholipids, and chemerin) from the placenta to maternal circulation, as well as a lower LDL uptake from circulation to placenta, eventually resulting in dyslipidemia in the patient (This figure with the credit “Created with BioRender.com.”)