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. 2023 Mar 13;55(3):628–642. doi: 10.1038/s12276-023-00962-w

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© The Author(s) 2023

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — A new EC subcluster marked by PLVAP expression with activating ANGPT and VEGF and PI3K-AKT pathway is unique in CM lesions. EndMT cells accompanied by strong immune activation were identified for the first time in CMs at the single-cell level. SPI1 is a novel key driver of EndMT. Trajectory analysis showed that typical SMCs (SMC2) gradually transdifferentiated into fibroblast-like SMCs (SMC1) in CM lesions. TWIST1 could induce SMC phenotypic switching.