Figure 3.

The current molecular mechanism of crosstalk among autophagy, apoptosis, and pyroptosis under silica circumstances. Two important members of the Bcl-2 apoptotic protein family, Bcl-2 and BBC3, activate autophagy via reducing the Bcl-2–BECN1 complex in silica-induced pulmonary fibrosis. Autophagy activity is also stimulated by silica-induced ER stress. Lysosomal disruption, a critical characteristic of silica-induced autophagy, could foster the formation of the NALP3–ASC complex. It further activates cas-1, boosting the transformation from pro-IL-1β to IL-1β and executing pyroptosis. Notably, the relationship between autophagy and NALP3 or the mechanism of cas-3-mediated pyroptosis deserves more exploration.