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. 2021 Dec 3;53(12):1866–1876. doi: 10.1038/s12276-021-00704-w

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© The Author(s) 2021

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. 3 — a t-SNE plots of the SMC subpopulations from control and hypertensive tissue (control, n = 1422 SMCs. hypertension, n = 1949 SMCs. SMC 1, n = 2296 cells; SMC 2, n = 874 cells; SMC 3, n = 202 cells). b Heatmap showing the top 10 genes (by average log(fold change)) for each SMC cell subpopulation. c Bar graph of the composition of each SMC subpopulation (dashed black line, expected proportion of cells in the control group). d Dot plots of typical SMC markers for 3 SMC subpopulations from the control. e Expression of contractile SMC markers for 3 SMC subpopulations from control and hypertensive tissue. ^***Mann–Whitney U test p < 0.001 vs. SMC 1, HighSalt. f Violin plots of the Klf4 gene associated with phenotypic modulation of SMCs. g The results of gene set enrichment analysis (GSEA) using a hallmark gene set showing enriched differentially expressed gene (DEG) counts between the control and hypertension groups.