HMGB1 promotes LPS-induced M1 polarization and apoptosis in microglia by mediating the expression of immune and inflammation-related genes

HMGB1 may drive microglia toward a pro-inflammatory M1 phenotype, thereby mediating neuroinflammatory damage in POCD, potentially through activation of STAT, TNF, and IL-17 signaling pathways. Targeting HMGB1 and its downstream genes (e.g., Ccl22, Lcn2, Stat5a, Tlr2, Cd74, Egr2) could provide effective diagnostic and interventional strategies for POCD.