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Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Updated: Apr 20, 2026

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Epigenetics in rheumatoid arthritis.

Kerstin Klein1, Steffen Gay

  • 1Center of Experimental Rheumatology, University Hospital Zurich, Zurich, Switzerland.

Current Opinion in Rheumatology
|November 22, 2014
PubMed
Summary

Epigenetic modifications like DNA methylation play a crucial role in rheumatoid arthritis (RA). Recent research highlights their connection to genetic and environmental factors, offering new therapeutic targets.

Area of Science:

  • Rheumatology
  • Epigenetics
  • Immunology

Background:

  • Rheumatoid arthritis (RA) pathogenesis involves complex interactions between genetic predisposition and environmental influences.
  • Epigenetic modifications, including DNA methylation and histone modifications, are increasingly recognized as key regulators in immune cell function and disease development.

Purpose of the Study:

  • To provide a comprehensive overview of recent scientific literature on the role of epigenetic modifications in rheumatoid arthritis (RA).
  • To specifically focus on DNA methylation and posttranslational histone modifications as investigated in recent studies.

Main Methods:

  • Systematic review of recently published articles.
  • Analysis of studies investigating DNA methylation patterns in RA.
  • Examination of research on posttranslational histone modifications in RA pathogenesis.

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Main Results:

  • Epigenetic modifications are linked to both genetic and environmental risk factors for RA.
  • Histone deacetylases mediate the impact of environmental factors (smoking, diet, therapy) on gene expression in RA.
  • Altered DNA methylation patterns and cell-type specific histone methylation marks are implicated in RA genetic risk.
  • Aberrant methylome signatures in RA synovial fibroblasts contribute to their activation.
  • Inhibition of the polyamine recycling pathway shows potential for reversing DNA hypomethylation and offers a novel epigenetic therapy for RA.
  • Targeting epigenetic reader proteins, such as bromodomain proteins, is a promising new avenue for drug development in autoimmune diseases.

Conclusions:

  • Epigenetic factors serve as a critical link connecting genetic susceptibility, gene expression regulation, and environmental triggers in RA.
  • Emerging epigenetic therapies targeting DNA methylation and reader proteins hold significant promise for managing RA and other autoimmune conditions.