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<p>Myocardial infarction (MI) induces ischemic damage, triggering endothelial cell (EC) dysfunction that impairs revascularization and cardiac recovery. A key contributor to this dysfunction is excessive endoplasmic reticulum (ER) stress, which is activated by MI and exacerbates EC apoptosis and impaired angiogenesis. Here we investigate the role of endothelial-specific protein arginine methyltransferase 7 (PRMT7) in mitigating ER stress and promoting vascular homeostasis after MI. We demonstrate that PRMT7 expression is upregulated in ECs under tumor necrosis factor α or tunicamycin treatment, while its inhibition exacerbates ER stress and induces EC death. Using endothelial-specific PRMT7-knockout models, we show that PRMT7 deficiency increases apoptosis and fibrosis, impairing cardiac recovery. Transcriptomic analysis reveals that PRMT7 loss leads to the upregulation of pro-apoptotic pathways and suppression of angiogenic and proliferative signaling. Conversely, PRMT7 overexpression or treatment with the PRMT7-inducing drug bindarit restores EC function, suppresses ER stress and enhances revascularization and cardiac repair after MI. These findings establish endothelial PRMT7 as a critical regulator of EC survival and function, highlighting its potential as a therapeutic target to mitigate ER stress and improve post-MI cardiac recovery.</p>

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Endothelial PRMT7 prevents dysfunction, promotes revascularization and enhances cardiac recovery post-myocardial infarction

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月5日

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  • Thi Thuy Vy Tran,
  • Yan Zhang,
  • Shibo Wei,
  • Jinwoo Lee,
  • Yideul Jeong,
  • Tuan Anh Vuong,
  • Sang-Jin Lee,
  • Dongryeol Ryu,
  • Gyu-Un Bae,
  • Jong-Sun Kang

摘要

Myocardial infarction (MI) induces ischemic damage, triggering endothelial cell (EC) dysfunction that impairs revascularization and cardiac recovery. A key contributor to this dysfunction is excessive endoplasmic reticulum (ER) stress, which is activated by MI and exacerbates EC apoptosis and impaired angiogenesis. Here we investigate the role of endothelial-specific protein arginine methyltransferase 7 (PRMT7) in mitigating ER stress and promoting vascular homeostasis after MI. We demonstrate that PRMT7 expression is upregulated in ECs under tumor necrosis factor α or tunicamycin treatment, while its inhibition exacerbates ER stress and induces EC death. Using endothelial-specific PRMT7-knockout models, we show that PRMT7 deficiency increases apoptosis and fibrosis, impairing cardiac recovery. Transcriptomic analysis reveals that PRMT7 loss leads to the upregulation of pro-apoptotic pathways and suppression of angiogenic and proliferative signaling. Conversely, PRMT7 overexpression or treatment with the PRMT7-inducing drug bindarit restores EC function, suppresses ER stress and enhances revascularization and cardiac repair after MI. These findings establish endothelial PRMT7 as a critical regulator of EC survival and function, highlighting its potential as a therapeutic target to mitigate ER stress and improve post-MI cardiac recovery.