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. 2017 Jul 25;8:519. doi: 10.3389/fphys.2017.00519

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Copyright © 2017 Luo, Huang, Liu, Liang, Wei, Ke, Zeng, Huang and He.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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NLRP3 inflammasome activation in DCM. Hyperglycemia-induced reactive oxygen species (ROS) leads to nuclear factor-kB (NF-κB) and TXNIP overexpression. NF-κB increases the expression of NLRP3, pro-IL-18, and pro-IL-1β. TXNIP modulates the biological structure of NLRP3 leading to NLRP3 inflammasome assembly and pro-caspase-1 (pro-casp-1) autocleavage. Active caspase-1 (Casp-1) promotes pro-IL-18 and pro-IL-1β maturation, which facilitate inflammatory reaction. On the other hand, active caspase-1 cleaves GSDMD within the linker between its N-terminal (blue) and C-terminal (magenta). The released GSDMD-N domain oligomerizes to generate membrane pores, which disrupts the osmotic potential and leads to cell swelling and eventual lysis.