Figure 3.

Microglia autophagy in the regulation of inflammatory responses in ischemic stroke. Microglial autophagy bidirectionally regulates inflammatory responses and there are complex interactions between them in ischemic stroke. The downregulation of Microglial PDE1-B, GSK-3β, and the upregulation of PARP14 promote microglia autophagy and suppress inflammatory responses. The upregulation of PGC-1α promotes autophagy and mitophagy via ULK1 and inhibits the overactivation of NLRP3 inflammasome. DJ-1 activates the Atg5-Atg12-Atg16L1 complex via Sirt1 and alleviates inflammatory responses. HIF-1 regulates the expression of BNIP3, induces autophagy by disrupting the interaction of Beclin1 with Bcl-2 and suppresses microglia inflammatory cytokine overexpression during early hypoxia. Activation of autophagy via the AMPK pathway can facilitate microglia alternatively activation and exert neuroprotective effects during an inflammatory process. P2X7 receptor can activate AMPK pathways in the regulation of mitochondrial and lysosomal functions in microglia. Sestrin2 promote microglia autophagy via inhibiting mTOR pathway to attenuate microglial inflammatory response. The upregulation of TRPV1 and CTRP1 inhibit autophagy and reduces the inflammatory response. MiR-30d-5p inhibits Beclin-1 and ATG5 expression and exerts an anti-inflammatory effect. Microglial PTP1B, SphK1, and TLR4 induce autophagy and promote microglial proinflammatory activation.