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. 2022 Jan 28;23:47. doi: 10.1186/s12882-021-02593-7

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© The Author(s) 2022

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 — Increase in plasma and cardiac cell expression and production of CXCL10 in human chronic kidney disease. A Heatmap showing mRNA expression fold change from healthy control in iPSC-derived cardiomyocytes (CM), human cardiac microvascular endothelial cells (EC) and primary ventricular fibroblasts (FB) treated with serum from healthy or CKD donors. Mean of two independent donors. B Heatmap showing protein secretion fold change from healthy control in supernatant of iPSC-CM, EC and FB treated with serum from CKD patients. Mean of two independent donors. C CKD patients or matched healthy controls were recruited and plasma levels of CXCL10 measured by ELISA. CKD patients were split into CKD stage 3, 4 or 5. Each individual donor was tested in triplicate. **** represents P < 0.0001 from healthy controls