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<p>The mammalian heart retains regenerative capacity during the early postnatal period, but this ability declines as it matures. Enhancing cardiomyocyte proliferation represents a key therapeutic approach to promote heart regeneration and repair, yet the molecular mechanisms remain elusive. Here, we identified <i>LncBAR</i> (BAF complex-associated lncRNA) as a critical regulator of cardiac regeneration. <i>LncBAR</i> expression declines during heart development but is upregulated following cardiac injury. Loss of <i>LncBAR</i> impairs cardiomyocyte growth, suppresses cell cycle gene expression, and diminishes heart regeneration, as evidenced by reduced cytokinesis and cardiac function. Conversely, cardiac specific overexpression of <i>LncBAR</i> restores cardiomyocyte proliferation and enhances cardiac regeneration, especially in adult myocardial infarction model. Mechanistically, <i>LncBAR</i> interacts with <i>Brg1</i>, stabilizing BRG1 protein level and activating cell cycle progression to drive cardiomyocytes proliferation. Collectively, our study identified <i>LncBAR</i> as a crucial regulator for heart regeneration, highlighting the <i>LncBAR</i>-BRG1 axis as a promising therapeutic strategy for cardiac repair.</p>

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Long noncoding RNA LncBAR enhances BRG1 protein to promote cardiomyocyte cell cycle progression and cardiac repair

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月17日

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  • Jun Li,
  • Huanhuan Cai,
  • Yufan Chen,
  • Ruiqi Pi,
  • Lilin Xiang,
  • Zhibing Lu,
  • Yan Zhou,
  • Li Wang

摘要

The mammalian heart retains regenerative capacity during the early postnatal period, but this ability declines as it matures. Enhancing cardiomyocyte proliferation represents a key therapeutic approach to promote heart regeneration and repair, yet the molecular mechanisms remain elusive. Here, we identified LncBAR (BAF complex-associated lncRNA) as a critical regulator of cardiac regeneration. LncBAR expression declines during heart development but is upregulated following cardiac injury. Loss of LncBAR impairs cardiomyocyte growth, suppresses cell cycle gene expression, and diminishes heart regeneration, as evidenced by reduced cytokinesis and cardiac function. Conversely, cardiac specific overexpression of LncBAR restores cardiomyocyte proliferation and enhances cardiac regeneration, especially in adult myocardial infarction model. Mechanistically, LncBAR interacts with Brg1, stabilizing BRG1 protein level and activating cell cycle progression to drive cardiomyocytes proliferation. Collectively, our study identified LncBAR as a crucial regulator for heart regeneration, highlighting the LncBAR-BRG1 axis as a promising therapeutic strategy for cardiac repair.