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. 2021 Aug 19;11(8):1239. doi: 10.3390/biom11081239

Figure 2.

Figure 2

Hypothetical mechanism for the role of NLRP3 in glaucoma. Activation of the NLRP3 inflammasome requires two signals for activation. Signal 1 results in transcriptional upregulation of Pro-IL-1β and NLRP3 protein via the NF-κβ pathway. Stress to the ONH is thought to activate the NF-κβ pathway. Signal 2 results in the oligomerisation of ASC, NLRP3, and pro-caspase-1 to form the NLRP3 inflammasome. NLRP3 inflammasome oligomerisation results in cleavage of pro-caspase-1 into active caspase-1, which can in turn cleave pro-IL-1β into IL-1β, which can leave the cell to drive inflammation. ROS or extracellular ATP are proposed to result in inflammasome oligomerisation in glaucoma. ONH—optic nerve head; ROS—reactive oxygen species; ATP—adenosine triphosphate; RGC—retinal ganglion cell; DAMPS—danger associated molecular patterns; IL-1β—interluekin-1beta; ASC—apoptosis-associated speck-like protein containing a caspase-recruitment domain; NLRP3—NLR family pyrin domain containing 3; NF-κβ—nuclear factor-kappa beta.