Fig. 8: Proposed model of endothelial pyroptosis in nicotine-promoted atherosclerosis.
From: Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis
Nicotine enters endothelial cell, and induces the production of ROS, which activates NLRP3 inflammasome, leading to the activation of caspase-1. Activated caspase-1 triggers pore formation of membrane, DNA fragmentation and release of mature IL-1β and IL-18 from cells, causing a sterile inflammation response, further contributing to the pyroptotic cell death and subsequent promoting atherosclerosis
