Fig. 3

CHI3L1 Interactions and Intracellular Signaling Pathways in Neuroinflammation and Tumor Progression. CHI3L1 interacts with various cell surface receptors, including IL-13Rα2, syndecan-1/αvβ3, and RAGE, triggering multiple intracellular signaling pathways. These interactions lead to diverse cellular outcomes, such as the regulation of apoptosis, tumor metastasis, inflammation, carcinogenesis, and tumor angiogenesis. Interaction with syndecan-1 induces angiogenesis through integrin αvβ3 and MAPK signaling. CHI3L1’s interaction with RAGE activates the Wnt/β-catenin pathway, promoting tumor progression by facilitating immune evasion and migration. Similarly, interactions with IL-13Rα2 drive carcinogenesis and tumor angiogenesis via Erk1/2, Wnt/β-catenin, and Akt signaling pathways. Additionally, CHI3L1 modulates brain inflammation and neurodegenerative disorders by influencing the IL-13 signaling pathway through IL-13Rα2, enhancing the secretion of inflammatory cytokines such as IL-1β and IL-6, and activating pathways like AKT and ERK1/2