Suggested by the idea that the structure of chromatin can be modified to allow or deny access of transcription activators, regulatory functions of histone acetylation and deacetylation can have implications with genes that cause other diseases. Studies on histone modifications may reveal many novel therapeutic targets.
Based on different cardiac hypertrophy models, it has been demonstrated that cardiac stress can result in gene expression changes and alter cardiac function. These changes are mediated through HATs/HDACs posttranslational modification signaling. HDAC inhibitor trichostatin A was reported to reduce stress induced cardiomyocyte autophagy. Studies on p300 and CREB-binding protein linked cardiac hypertrophy with cellular HAT activity suggesting an essential role of histone acetylation status with hypertrophy responsive genes such as GATA4, SRF, and MEF2.
Epigenetic modifications also play a role in neurological disorders. Deregulation of histones modification are found to be responsible for deregulated gene expression and hence associated with neurological and psychological disorders, such as Schizophrenia and Huntington disease. Current studies indicate that inhibitors of the HDAC family have therapeutic benefits in a wide range of neurological and psychiatric disorders. Many neurological disorders only affect specific brain regions; therefore, understanding of the specificity of HDACs is still required for further investigations for improved treatments.