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MT-dependent Rho activation plays a critical role in ROS-induced endothelial dysfunction. An increase in ROS levels activates HDAC6, which causes MT destabilization and release of MT-bound GEF-H1. The subsequent activation of Rho then mediates an increase in endothelial permeability as well as EC inflammatory responses. HDAC6, histone deacetylase 6; MT, microtubules.
