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<p>Acute myocardial infarction (AMI) triggers a robust inflammatory response in which macrophage polarization critically influences cardiac repair, yet the regulatory role of microRNAs remains largely undefined. Through integrated analysis of GEO datasets and experimental validation in hypoxic Raw264.7 cells and a mouse AMI model, we identified that miR-378a-3p is significantly downregulated following ischemic injury. Administration of miR-378a-3p mimics in vitro or miR-378a-3p agomir in vivo suppressed M1 macrophage polarization, attenuated inflammatory cytokine production, and markedly improved cardiac function and remodeling after AMI. Mechanistically, miR-378a-3p directly bound the 3’UTR of Trem1 mRNA, and Trem1 overexpression reversed the anti-inflammatory effects of miR-378a-3p, confirming Trem1 as a functional target. This study unveils the miR-378a-3p/Trem1 axis as a critical regulator of post-infarction inflammation and identifies miR-378a-3p as a promising therapeutic candidate for mitigating acute cardiac injury and improving outcomes in AMI patients.</p> Graphical Abstract <p>Schematic diagram illustrating the proposed mechanism by which miR-378a-3p promotes post-myocardial infarction repair by regulating macrophage polarization.</p> <p></p>

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MiR-378a-3p Promotes Macrophage Polarization from M1 to M2 for Cardiac Repair after Infarction Via Trem1

  • 期刊论文

  • 发表日期：

    2026年7月11日

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  • Ming Shen,
  • Tongxuan Li,
  • Xuan Jiang,
  • Zichang Wang,
  • Ningbo Liu,
  • Peihong Wu,
  • Gang Wang,
  • Mingqi Zheng

摘要

Acute myocardial infarction (AMI) triggers a robust inflammatory response in which macrophage polarization critically influences cardiac repair, yet the regulatory role of microRNAs remains largely undefined. Through integrated analysis of GEO datasets and experimental validation in hypoxic Raw264.7 cells and a mouse AMI model, we identified that miR-378a-3p is significantly downregulated following ischemic injury. Administration of miR-378a-3p mimics in vitro or miR-378a-3p agomir in vivo suppressed M1 macrophage polarization, attenuated inflammatory cytokine production, and markedly improved cardiac function and remodeling after AMI. Mechanistically, miR-378a-3p directly bound the 3’UTR of Trem1 mRNA, and Trem1 overexpression reversed the anti-inflammatory effects of miR-378a-3p, confirming Trem1 as a functional target. This study unveils the miR-378a-3p/Trem1 axis as a critical regulator of post-infarction inflammation and identifies miR-378a-3p as a promising therapeutic candidate for mitigating acute cardiac injury and improving outcomes in AMI patients.

Graphical Abstract

Schematic diagram illustrating the proposed mechanism by which miR-378a-3p promotes post-myocardial infarction repair by regulating macrophage polarization.