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This regulatory mechanism is corroborated by findings in myocardial injury models: miR-182 promotes M2 polarization via the TLR4/NF-κB/PI3K signaling axis, thereby improving myocardial ischemia–reperfusion injury (133), whereas miR-155 promotes M1 polarization through TLR signaling, exacerbating myocardial inflammation (134), collectively highlighting a conserved role of miRNAs in regulating macrophage polarization