Updating a Strategy for Histone Deacetylases and Its Inhibitors in the Potential Treatment of Cerebral Ischemic Stroke

Figure 1

Overview of the probable mechanism between HDACs and their inhibitors. Due to the different distributions of HDACs in the cytoplasm and nuclei, the related mechanisms of cerebral ischemia show the different types. When cerebral infraction occurred, HDAC 1 and 2 in the nucleus were released into the cytoplasm that caused homeostasis of the cellular environment to be destroyed. It will continuously lead to the degradation of DNA. Meanwhile, HDAC 3, 4, 5, and 9 would participate in apoptosis, inflammation response, and Golgi apparatus dysfunction as well as autophagy, which is particularly apparent in HDAC9, respectively. Moreover, HDAC NAD⁺-dependent class III (SIRT1) could aggravate the ischemic injury p53 acetylation and NF-κB.