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<p>Despite advances in reperfusion therapy, treatment outcomes for myocardial infarction (MI) remain limited by poor targeting specificity and insufficient bioavailability of therapeutic agents in the ischemic myocardium. Here, we report CCTP-miR@CTP, a non-liposomal nanozyme platform that integrates cardiomyocyte-targeted delivery, intrinsic catalytic antioxidant activity, and therapeutic miRNA delivery within a single multifunctional system. In vitro, CCTP loaded with miR-26a mitigated H₂O₂-induced ROS accumulation, restored mitochondrial membrane potential, and suppressed autophagy and apoptosis in cardiomyocytes. In vivo, CCTP-miR@CTP preferentially accumulated in the infarcted myocardium, where it reduced infarct size, improved cardiac function, suppressed inflammatory responses, promoted angiogenesis, and attenuated extracellular matrix deposition and myocardial fibrosis. Mechanistically, CCTP not only served as an effective nucleic acid carrier but also coordinated redox homeostasis and cell survival pathways, amplifying the therapeutic efficacy of miRNA-based intervention. This study presents a material-design strategy to improve miRNA druggability in cardiovascular medicine and identifies CCTP-miR@CTP as a candidate nanotherapeutic for MI.</p> Graphical Abstract <p></p>

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Cardiac-targeted delivery of miRNA via antioxidant nanozymes ameliorates cardiac dysfunction and fibrosis after myocardial infarction

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月3日

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  • Tong Yu,
  • Jingyi Gong,
  • Ping Pang,
  • Jun Ma,
  • Mengjia Wang,
  • Jiahao Ding,
  • Xinjie Zhou,
  • Haoshu Wang,
  • Zhiyi Yin,
  • Gulizhaer Ainiwa,
  • Xiuni He,
  • Shuxia Jiang,
  • Damin Ding,
  • Huixia Xuan,
  • Yu Luo,
  • Kaiyang Wang,
  • Hongli Shan

摘要

Despite advances in reperfusion therapy, treatment outcomes for myocardial infarction (MI) remain limited by poor targeting specificity and insufficient bioavailability of therapeutic agents in the ischemic myocardium. Here, we report CCTP-miR@CTP, a non-liposomal nanozyme platform that integrates cardiomyocyte-targeted delivery, intrinsic catalytic antioxidant activity, and therapeutic miRNA delivery within a single multifunctional system. In vitro, CCTP loaded with miR-26a mitigated H₂O₂-induced ROS accumulation, restored mitochondrial membrane potential, and suppressed autophagy and apoptosis in cardiomyocytes. In vivo, CCTP-miR@CTP preferentially accumulated in the infarcted myocardium, where it reduced infarct size, improved cardiac function, suppressed inflammatory responses, promoted angiogenesis, and attenuated extracellular matrix deposition and myocardial fibrosis. Mechanistically, CCTP not only served as an effective nucleic acid carrier but also coordinated redox homeostasis and cell survival pathways, amplifying the therapeutic efficacy of miRNA-based intervention. This study presents a material-design strategy to improve miRNA druggability in cardiovascular medicine and identifies CCTP-miR@CTP as a candidate nanotherapeutic for MI.

Graphical Abstract