The DOI matches its Crossref record; 262 of the 264 references it cites were found in a registry or an index.
Role of Epigenetics in Inflammation-Associated Diseases
Abstract
There is considerable evidence suggesting that epigenetic mechanisms may mediate development of chronic inflammation by modulating the expression of pro-inflammatory cytokine TNF-α, interleukins, tumor suppressor genes, oncogenes and autocrine and paracrine activation of the transcription factor NF-κB. These molecules are constitutively produced by a variety of cells under chronic inflammatory conditions, which in turn leads to the development of major diseases such as autoimmune disorders, chronic obstructive pulmonary diseases, neurodegenerative diseases and cancer. Distinct or global changes in the epigenetic landscape are hallmarks of chronic inflammation driven diseases. Epigenetics include changes to distinct markers on the genome and associated cellular transcriptional machinery that are copied during cell division (mitosis and meiosis). These changes appear for a short span of time and they necessarily do not make permanent changes to the primary DNA sequence itself. However, the most frequently observed epigenetic changes include aberrant DNA methylation, and histone acetylation and deacetylation. In this chapter, we focus on pro-inflammatory molecules that are regulated by enzymes involved in epigenetic modifications such as arginine and lysine methyl transferases, DNA methyltransferase, histone acetyltransferases and histone deacetylases and their role in inflammation driven diseases. Agents that modulate or inhibit these epigenetic modifications, such as HAT or HDAC inhibitors have shown great potential in inhibiting the progression of these diseases. Given the plasticity of these epigenetic changes and their readiness to respond to intervention by small molecule inhibitors, there is a tremendous potential for the development of novel therapeutics that will serve as direct or adjuvant therapeutic compounds in the treatment of these diseases.
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“It has also been reported that there is positive regulation of miRNA-510, as well as negative regulation of miRNA-342 and 191, which contribute to the development of the disease [90,91].”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [91]
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“In other diseases such as diabetes, increased levels of histone methylations have been identified in the promoter of CLT4, a gene highly susceptible to type 1 diabetes that has been correlated with the activation of T cells.”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [91]
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Metadata
- Authors
- Shanmugam, M. K., & Sethi, G.
- Affiliations
- National University of Singapore (SG)
- Corresponding author
- Sethi, Gautam
- Venue
- Subcellular Biochemistry
- Publisher
- Springer Netherlands
- Published
- 2012-06-28
- Volume
- 61
- Pages
- 627-657
- ISSN
- 0306-0225 (ISSN-L)
- OpenAlex
- W164032219
- Cited by
- 141
- References
- 264
- Citations by year
- 2026: 2 · 2025: 12 · 2024: 7 · 2023: 13 · 2022: 8 · 2021: 9 · 2020: 12 · 2019: 15 · 2018: 8 · 2017: 9 · 2016: 15 · 2015: 13 · 2014: 8 · 2013: 10
- FWCI
- 16.97
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Sub-cellular biochemistry/Subcellular biochemistry (publishedVersion)
- PubMed (publishedVersion)
- National University of Singapore (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Keywords
- epigenetics, chronic inflammation, inflammation-associated diseases, DNA methylation, histone acetylation, histone deacetylation, NF-κB, TNF-α, interleukins, histone methyltransferase, DNA methyltransferases, histone acetyltransferase, histone deacetylase inhibitors, histone acetyltransferase inhibitors, autoimmune disease, chronic obstructive pulmonary disease, neurodegenerative diseases, cancer, epigenetic therapy
- MeSH terms
- Animals, Anti-Inflammatory Agents, Gene Expression Regulation, Humans, Inflammation, Phenotype, Cytokines, Inflammation Mediators, Genetic Predisposition to Disease, Epigenesis, Genetic, Molecular Targeted Therapy
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