Abstract
Endothelial tight junction disruption in diabetes requires Nlrp3 inflammasomes. High glucose activates Nlrp3 inflammasome in endothelial cells via ROS production. Activation of endothelial inflammasome by high glucose triggers release of HMGB1. Blockade of Nlrp3/HMGB1 axis inhibits high glucose-induced endothelial permeability.
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