title: Epigenetic dysfunctional diseases and therapy for infection and inflammation.
abstract: Even though the discovery of the term 'epigenetics' was in the 1940s, it has recently become one of the most promising and expanding fields to unravel the gene expression pattern in several diseases. The most well studied example is cancer, but other diseases like metabolic disorders, autism, or inflammation-associated diseases such as lung injury, autoimmune disease, asthma, and type-2 diabetes display aberrant gene expression and epigenetic regulation during their occurrence. The change in the epigenetic pattern of a gene may also alter gene function because of a change in the DNA status. Constant environmental pressure, lifestyle, as well as food habits are the other important parameters responsible for transgenerational inheritance of epigenetic traits. Discovery of epigenetic modifiers targeting DNA methylation and histone deacetylation enzymes could be an alternative source to treat or manipulate the pathogenesis of diseases. Particularly, the combination of epigenetic drugs such as 5-aza-2-deoxycytidine (Aza) and trichostatin A (TSA) are well studied to reduce inflammation in an acute lung injury model. It is important to understand the epigenetic machinery and the function of its components in specific diseases to develop targeted epigenetic therapy. Moreover, it is equally critical to know the specific inhibitors other than the widely used pan inhibitors in clinical trials and explore their roles in regulating specific genes in a more defined way during infection.
authors.affiliation: Department of Internal Medicine, Cardiovascular Research Institute, University of Kansas Medical Center, Kansas City, KS, USA.
authors.forename: Saheli
authors.initials: S
authors.lastname: Samanta
authors.affiliation: Department of Internal Medicine, Cardiovascular Research Institute, University of Kansas Medical Center, Kansas City, KS, USA.
authors.forename: Sheeja
authors.initials: S
authors.lastname: Rajasingh
authors.affiliation: Department of Internal Medicine, Cardiovascular Research Institute, University of Kansas Medical Center, Kansas City, KS, USA.
authors.forename: Thuy
authors.initials: T
authors.lastname: Cao
authors.affiliation: Department of Internal Medicine, Cardiovascular Research Institute, University of Kansas Medical Center, Kansas City, KS, USA.
authors.forename: Buddhadeb
authors.initials: B
authors.lastname: Dawn
authors.affiliation: Department of Internal Medicine, Cardiovascular Research Institute, University of Kansas Medical Center, Kansas City, KS, USA; Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, KS, USA. Electronic address: rjohnson9@kumc.edu.
authors.forename: Johnson
authors.initials: J
authors.lastname: Rajasingh
mesh_terms: D000818:Animals; D003141:Communicable Diseases / Q000188:drug therapy / Q000235:genetics*; D019175:DNA Methylation / Q000187:drug effects; D055808:Drug Discovery; D044127:Epigenesis, Genetic / Q000187:drug effects; D042421:Histone Code / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000235:genetics*; D035683:MicroRNAs / Q000235:genetics
chemical_list: D035683:MicroRNAs
keywords: 5-Aza-2-deoxycytidine; DNA methyl transferase; Epigenetic modifier; Histone deacetylase; Inflammation; Trichostatin A