• Xue Peng, Hengmei Chen, Yunyun Li, Dake Huang, Baojun Huang, and Dengqun Sun.
• Department of Pathology, Anhui Armed Police General Hospital, Hefei, 230032, Anhui, China.
• Cell Biol. Int. 2020 Jul 1; 44 (7): 1481-1490.

AbstractPyroptosis is a form of cell death that is uniquely dependent on caspase-1. Pyroptosis involved in oxidized low-density lipoprotein (ox-LDL)-induced human macrophage death through the promotion of caspase-1 activation is important for the formation of unstable plaques in atherosclerosis. The mitochondrial outer membrane protein NIX directly interacts with microtubule-associated protein 1 light chain 3 (LC3). Although we previously showed that NIX-mediated mitochondrial autophagy is involved in the clearance of damaged mitochondria, how NIX contributes to ox-LDL-induced macrophage pyroptosis remains unknown. Here, immunoperoxidase staining Nix expression decreased in human atherosclerosis. When we silenced NIX expression in murine macrophage cell, active caspase-1, and mature interleukin-1β expression levels were increased and LC3 was reduced. In addition, LDH release and acridine orange and ethidium bromide staining indicated that damage to macrophage cell membranes induced by ox-LDL was substantially worse. Moreover, intracellular reactive oxygen species and NLRP3 inflammasome levels increased. Taken together, these results demonstrated that NIX inhibits ox-LDL-induced macrophage pyroptosis via autophagy in atherosclerosis.© 2020 International Federation for Cell Biology.

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