Wnt1 oversees microglial activation by the Wnt/LRP5/6 receptor signaling pathway during lipopolysaccharide-mediated toxicity

CONCLUSIONS: The anti-inflammatory effects of Wnt1 on BV2 cells improved autophagy, a mechanism partly dependent on the β-catenin pathway or the phosphorylation of LKB1. Furthermore, the Wnt1/LKB1 pathway was activated independently of β-catenin and participated in regulating its expression. Our research unveils a previously unknown method through which Wnt1 exerts its anti-inflammatory effects, which may have a potential protective role against CNS diseases.