HDAC5 and cardiovascular disorder: Agonist (e.g., AngII)-mediated activation of AT1R has been reported to induce the nuclear mobilization of TFs, including GATA binding protein (GATA4), nuclear factor of activated T cells (NFAT), signal transducer and activator of transcription 3 (STAT3), nuclear factor-kappaB (NF-κB), extracellular signal-regulated kinases (ERK1/2), protein kinase C and HDAC5, during the progression of cardiovascular diseases [22]–[27].