作者: Muthu K. Shanmugam , Gautam Sethi
DOI: 10.1007/978-94-007-4525-4_27
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摘要: There is considerable evidence suggesting that epigenetic mechanisms may mediate development of chronic inflammation by modulating the expression pro-inflammatory cytokine TNF-α, interleukins, tumor suppressor genes, oncogenes and autocrine paracrine activation transcription factor NF-κB. These molecules are constitutively produced a variety cells under inflammatory conditions, which in turn leads to major diseases such as autoimmune disorders, obstructive pulmonary diseases, neurodegenerative cancer. Distinct or global changes landscape hallmarks driven diseases. Epigenetics include distinct markers on genome associated cellular transcriptional machinery copied during cell division (mitosis meiosis). appear for short span time they necessarily do not make permanent primary DNA sequence itself. However, most frequently observed aberrant methylation, histone acetylation deacetylation. In this chapter, we focus regulated enzymes involved modifications arginine lysine methyl transferases, methyltransferase, acetyltransferases deacetylases their role Agents modulate inhibit these modifications, HAT HDAC inhibitors have shown great potential inhibiting progression Given plasticity readiness respond intervention small molecule inhibitors, there tremendous novel therapeutics will serve direct adjuvant therapeutic compounds treatment