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

ABSTRACT: 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 reco

SUBMITTER: Tran TTV 

PROVIDER: S-EPMC12411622 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature