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. 2023 Apr 26;13:6821. doi: 10.1038/s41598-023-32293-1

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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 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/.

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Single-nuclei RNA sequencing shows that ^CCND2hiPSC-MI cardiomyocytes increase cycling and upregulated HIPPO/YAP & MAPK signaling pathways, especially 7 days after MI injury. (A) Percentage of cardiomyocytes highly expressing cytokinesis-specific genes AURKB, ALKBH4, ANLN, CNTROB, and KLHDC8B in each group. (B–D) Bar graphs: sparse analysis quantifies the G2M phase, HIPPO/YAP, and MAPK signaling pathways in each heart; here, the sparse model only used DNA synthesis genes to compute a 'sparse model score' for each cell such that the score optimally separates fetal from naïve-P56 cardiomyocytes; a higher score implies more active G2M, HIPPO/YAP and MAPK activities. Each dot is the percentage of cells having 'high model score' in a heart. (E) Error bar: YAP1 average expression, which was per cell in each group; here, the raw counts were logarithm (base 2) transformed and scaled according to the total of UMIs and detected genes per cell by Seurat³⁰.