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In the context demyelination, the transient receptor potential vanilloid 1 (TRPV1) is needed to facilitate the efficient clearance of myelin debris, a process that paves the way for subsequent remyelination. By employing loss-of-function and gain-of-function studies, we revealed that microglial function is highly affected in terms of the functional activity of TRPV1. Global activation of TRPV1 drives microglia to demyelinating sites and enhances microglial phagocytosis, whereas TRPV1-deficient microglia failed to do so. The scavenger receptor CD36 mediates the enhanced phagocytosis following TRPV1 activation in microglia, accompanied by potential metabolic shift with downregulation of glycolysis.