Cited by 142Epigenetics and DNA MethylationGenomics and Chromatin DynamicsHistone Deacetylase Inhibitors Research

Role of Epigenetics in Inflammation-Associated diseases

Shanmugam, Muthu K., Sethi, Gautam·2013·Subcellular Biochemistry

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.

Integrity signals

Registry

Crossref · 10.1007/978-94-007-4525-4_27

Cites

262 of 262 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • Positive regulation of miRNA-510 and negative regulation of miRNA-342 and 191 contribute to the development of diabetes.

    “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].”
  • In diabetes, increased levels of histone methylations have been identified in the promoter of CLT4, a gene highly susceptible to type 1 diabetes, and correlated with the activation of T cells.

    “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.”

Cites

Flagged first, then by citations

2 of the 264 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Shanmugam, M. K., & Sethi, G.
Affiliations
National University of Singapore (SG)
Corresponding author
Sethi, Gautam
Venue
Subcellular Biochemistry
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