HIF1A and infection: On the one hand, HIPPE‐QU eradicated the local infection, removing the source of persistent immune stimulation and thereby significantly alleviating periodontal inflammation; on the other hand, the sustained release of QU and Cu2+ directly reprogrammed macrophage metabolism by modulating key intracellular pathways (such as HIF‐1–mediated glycolysis and controlled ROS generation), which shifted macrophage polarization from a pro‐inflammatory M1 phenotype to an anti‐inflammatory M2 phenotype and reshaped the immune microenvironment to favor tissue regeneration.