Novel Therapeutic Strategies for Ischemic Stroke: Recent Insights into Autophagy

Figure 2

Manipulation of autophagy in microglia after ischemic stroke. CTRP1 inhibits microglia autophagy and inflammation response by regulating the Akt/mTOR pathway after IS [88]. Microglia-specific PGC-1α activates autophagy through promoting the expression of ULK1 in an ERRα-dependent manner, thereby suppressing neuroinflammation [90]. Inhibition of PTPIB mitigates microglial activation by inhibiting PERK/eIF2α-dependent autophagy after ischemic stroke [87]. A proteolytic relay through the early CatE/TRAIL-dependent proteasomal and late CatB-dependent autophagic pathways for NF-κB activation plays an essential role in the neurotoxic polarization of microglia following ischemic stroke [83]. Geniposide and progesterone inhibits NLRP3 inflammasome activation via suppression autophagy in microglial cells in OGD and ischemic brain injury models [92, 93].