2020 Volume 14 Issue 2 Pages 74-82
NLRP3 inflammasome plays an essential role in innate immunity, yet the activation mechanism of NLRP3 inflammasome is not clear. In human or animal models, inappropriate NLRP3 inflammasome activation is implicated in many NLRP3-related diseases, such as tumors, inflammatory diseases and autoimmune diseases. Until now, a great number of inhibitors have been used to disturb the related signaling pathways, such as IL-1β blockade, IL-18 blockade and caspase-1 inhibitors. Unfortunately, most of these inhibitors just disturb the signaling pathways after the activation of NLRP3 inflammasome. Inhibitors that directly regulate NLRP3 to abolish the inflammation response may be more effective. NEK7 is a multifunctional kinase affecting centrosome duplication, mitochondrial regulation, intracellular protein transport, DNA repair and mitotic spindle assembly. Researchers have made significant observations on the regulation of gene transcription or protein expression of the NLRP3 inflammasome signaling pathway by NEK7. Those signaling pathways include ROS signaling, potassium efflux, lysosomal destabilization, and NF-κB signaling. Furthermore, NEK7 has been proved to be involved in many NLRP3-related diseases in humans or in animal models. Inhibitors focused on NEK7 may regulate NLRP3 to abolish the inflammation response and NEK7 may be a potential therapeutic target for NLRP3-related diseases.