Editorial Volume 11, Issue 16 pp 5871—5873

Fyn amplifies NLRP3 inflammasome signaling in Parkinson's disease

Figure 1. Role of Fyn in misfolded α-synuclein (αSyn)-mediated NLRP3 inflammasome activation. Left panel: The typical activation mechanism of the NLRP3 inflammasome, wherein disparate priming and activating signals are required for NLRP3 inflammasome assembly. The priming signal activates the NFκB pathway, leading to the elevated expression of NLRP3 and pro-IL-1β. The activation signal causes the release of mitoROS, which triggers inflammasome assembly, leading to cleavage of pro-IL-1β to IL-1β, which gets secreted. Right panel: αSyn can prime the NLRP3 inflammasome via CD36-Fyn-PKCδ signaling, which is required for NFκB activation, and can activate the NLRP3 inflammasome upon its uptake mediated by CD36 and Fyn.