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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
In the citing paper
“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]
Citations
Cites
Hanahan, D., & Weinberg, R. A. (2000) · Cell · doi:10.1016/s0092-8674(00)81683-9 · Cited by 29,219
Coussens, L. M., & Werb, Z. (2002) · Nature · doi:10.1038/nature01322 · Cited by 15,111
Mantovani, A., Allavena, P., Sica, A., & Balkwill, F. (2008) · Nature · doi:10.1038/nature07205 · Cited by 11,399
Inflammation and cancer: back to Virchow?
Balkwill, F., & Mantovani, A. (2001) · The Lancet · doi:10.1016/s0140-6736(00)04046-0 · Cited by 7,746
DNA methylation patterns and epigenetic memory
Bird, A. (2002) · Genes & Development · doi:10.1101/gad.947102 · Cited by 7,124
Jaenisch, R., & Bird, A. (2003) · Nature Genetics · doi:10.1038/ng1089 · Cited by 6,325
Death Receptors: Signaling and Modulation
Ashkenazi, A., & Dixit, V. M. (1998) · Science · doi:10.1126/science.281.5381.1305 · Cited by 5,866
The fundamental role of epigenetic events in cancer
Jones, P. A., & Baylin, S. B. (2002) · Nature Reviews Genetics · doi:10.1038/nrg816 · Cited by 5,648
Hypoxia — a key regulatory factor in tumour growth
Harris, A. L. (2002) · Nature Reviews Cancer · doi:10.1038/nrc704 · Cited by 5,177
Histone demethylation mediated by the nuclear amine oxidase homolog LSD1
Shi, Y., Lan, F., Matson, C., Mulligan, P., Whetstine, J. R., Cole, P. A., Casero, R. A., & Shi, Y. (2004) · Cell · doi:10.1016/j.cell.2004.12.012 · Cited by 4,051
Cited by
Sorted by citations
The Multifaceted Role of Curcumin in Cancer Prevention and Treatment
Shanmugam, M. K., Rane, G., Kanchi, M. M., Arfuso, F., Chinnathambi, A., Zayed, M. E., Alharbi, S. A., Tan, B. K. H., Kumar, A. P., & Sethi, G. (2015) · Molecules · doi:10.3390/molecules20022728 · Cited by 522
Self-citationOrtega, M. A., Fraile‐Μartinez, O., Montero, C. G., Álvarez-Mon, M. Á., Chaowen, C., Ruiz-Grande, F., Pekarek, L., Monserrat, J., Asúnsolo, Á., García‐Honduvilla, N., et al. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10153239 · Cited by 253
Molecular mechanisms of action of hesperidin in cancer: Recent trends and advancements
Aggarwal, V., Tuli, H. S., Thakral, F., Singhal, P., Aggarwal, D., Srivastava, S., Pandey, A., Sak, K., Varol, M., Khan, M. A., et al. (2020) · Experimental Biology and Medicine · doi:10.1177/1535370220903671 · Cited by 245
Self-citationMechanism of epithelial‐mesenchymal transition in cancer and its regulation by natural compounds
Ang, H. L., Mohan, C. D., Shanmugam, M. K., Leong, H. C., Makvandi, P., Rangappa, K. S., Bishayee, A., Kumar, A. P., & Sethi, G. (2023) · Medicinal Research Reviews · doi:10.1002/med.21948 · Cited by 234
Self-citationInnate Immune Programing by Endotoxin and Its Pathological Consequences
Morris, M. C., Gilliam, E. A., & Li, L. (2015) · Frontiers in Immunology · doi:10.3389/fimmu.2014.00680 · Cited by 224
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
