Key result
miR-378a-3p improves post-AMI cardiac function and remodeling by suppressing M1 macrophage polarization via Trem1.
Why the study?
Macrophage polarization critically influences cardiac repair after acute myocardial infarction, but the regulatory role of microRNAs remains largely undefined.
Does miR-378a-3p administration improve cardiac repair and reduce inflammation after acute myocardial infarction in preclinical models?
Does miR-378a-3p administration improve cardiac repair and reduce inflammation after acute myocardial infarction in preclinical models?
miR-378a-3p promotes cardiac repair post-myocardial infarction by shifting macrophage polarization from M1 to M2 via targeting Trem1, presenting a potential therapeutic target for AMI.
Answers are grounded in this paper and cite their sources.
Should not yet alter AMI management; leaves open miR-378a-3p as a research target for cardiac repair.
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.
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Shen et al. (2026) studied Acute myocardial infarction (AMI). miR-378a-3p mimics or agomir was evaluated on Macrophage polarization, inflammatory cytokine production, and cardiac function/remodeling. Administration of miR-378a-3p suppressed M1 macrophage polarization, attenuated inflammatory cytokine production, and markedly improved cardiac function and remodeling after AMI via Trem1.
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