Figure 8.

Schematic of TAZ regulation in the inflammatory response

After shuttling into the nucleus, TAZ might drive transcription of Nrf2 by interacting with the TEAD transcription factor and induce nc translocation of Nrf2 to enhance antioxidant capacity with reduction of intracellular ROS, resulting in impediment of NF-κB activation to ameliorate the microglia-mediated inflammatory response. Simultaneously, TAZ rescued microglia from apoptosis by preventing mitochondrial dysfunction, followed by blockage of mPTP opening and Cyt C release from mitochondria into the cytosol.