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BACKGROUND Accumulating studies in recent years have revealed that platelet activation is an important factor inducing neutrophil extracellular traps (NETs) formation in vivo, while the mechanism of this process is not fully elaborated, restricting its clinical use. Our previous study found that a histone deacetylase inhibitor (HDACi) could attenuate serum H3 elevation in septic mice, which was related to NETs formation, and others found HDAC6 to be involved in platelet activation, indicating that HDACis may attenuate platelet activatio
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