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<p>LVNC (Left Ventricular Non-Compaction), which is a type of cardiomyopathy characterized by an abnormal heart muscle structure. Retinoic acid (RA) is crucial for normal heart development, including the regulation of myocardial differentiation and chamber formation. <i>Cyp26b1</i> plays a key role in regulating RA signaling by degrading RA. However, more targeted research is needed to directly link <i>Cyp26b1</i> with LVNC pathology. To explore the effect of <i>Cyp26b1</i> on heart development, we collected heart tissues from wild type (WT) and <i>Cyp26b1</i> knockout (KO) mice at four time points (E10.5-E13.5) and performed single-cell RNA sequencing. We obtained 134,499 high-quality cells (57,923 WT and 62,488 KO) after filtering. The data quality was confirmed through various evaluation index and analytical methods mapping rates. Our initial analysis identified 10 major cell types in hearts, and differential expression analysis revealed the transcriptional change after deletion of <i>Cyp26b1</i>, particularly in cardiomyocytes. Collectively, these data offer a valuable resource for researchers investigating the role of <i>Cyp26b1</i> in heart development.</p>

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Single-cell RNA sequencing dataset of hearts from wild type and Cyp26b1 knockout mouse embryos

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月9日

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  • Zhao Zhang,
  • Xueting Chen,
  • Shuxin Su,
  • Silian Chen,
  • Li Pang,
  • Juan Shen,
  • Xiaodong Fang,
  • Zhe Zhang

摘要

LVNC (Left Ventricular Non-Compaction), which is a type of cardiomyopathy characterized by an abnormal heart muscle structure. Retinoic acid (RA) is crucial for normal heart development, including the regulation of myocardial differentiation and chamber formation. Cyp26b1 plays a key role in regulating RA signaling by degrading RA. However, more targeted research is needed to directly link Cyp26b1 with LVNC pathology. To explore the effect of Cyp26b1 on heart development, we collected heart tissues from wild type (WT) and Cyp26b1 knockout (KO) mice at four time points (E10.5-E13.5) and performed single-cell RNA sequencing. We obtained 134,499 high-quality cells (57,923 WT and 62,488 KO) after filtering. The data quality was confirmed through various evaluation index and analytical methods mapping rates. Our initial analysis identified 10 major cell types in hearts, and differential expression analysis revealed the transcriptional change after deletion of Cyp26b1, particularly in cardiomyocytes. Collectively, these data offer a valuable resource for researchers investigating the role of Cyp26b1 in heart development.