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In atherosclerotic plaques, MG-derived AGEs, including MG-H1 and THP, are detected, with MG-H1 specifically linked to rupture-prone plaque phenotypes [113] (Figure 4)

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Additionally, Lf can trigger α and β interferon (IFN) expression by intracellular signals and Lf receptors, which also hinders viral replication inside the host cell (Figure 1) [18]