Fig. 2

The molecular mechanism of microglial activation by galectin-3 (Gal-3). a Gal-3 activates microglia via IFN-γ and further induces the production of proinflammatory cytokines via the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway. b Gal-3 binds to microglial Toll-like receptor 4 (TLR4), triggering a proinflammatory response under acute neuroinflammatory conditions. c Gal-3 prevents lipopolysaccharide (LPS) from interacting with TLR4 by preferentially binding to LPS, which inhibits downstream proinflammatory cytokine production. d Gal-3/insulin-like growth factor 1 receptor (IGFR-1) interaction activates the IGF-mediated JAK/STAT pathway and microglial proliferation. e After secretion of sialidase to eliminate sialic acid from cell surface glycoproteins, Gal-3 binds the phagocytic receptor Mer tyrosine kinase (MerTK) and then contributes to phagocytosis by microglia. f Gal-3 interacts with advanced glycosylation end products (AGEs) to degrade its toxicity by fusing lysosomes