HMGB1 and stroke disorder: Similarly, HDAC4 and HDAC5 increased a cell viability through an inhibition of HMGB1, a central mediator of tissue damage following acute injury and it has been shown that NADPH oxidase-mediated HDAC4 and HDAC5 expression contributed to the cerebral ischemia injury through the HMGB1 signaling pathway that could be an effective therapeutic target to treat stroke (He et al., 2013).