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Cited by 79Epigenetics and DNA MethylationGenomics and Chromatin DynamicsGenetic Associations and Epidemiology

Epigenetics of chronic inflammatory diseases

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Stylianou, Eleni·2018·Journal of Inflammation Research
DOI 10.2147/jir.s129027PMC PMC6304253
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Abstract

Chronic, noncommunicable, and inflammation-associated diseases remain the largest cause of morbidity and mortality globally and within the United States. This is mainly due to our limited understanding of the molecular mechanisms that underlie these complex pathologies. The available evidence indicates that studies of epigenetics (traditionally defined as the heritable changes to gene expression that are independent of changes to DNA) are significantly advancing our knowledge of these inflammatory conditions. This review will focus on epigenetic studies of three diseases, that are among the most burdensome globally: cardiovascular disease, the number one cause of deaths worldwide, type 2 diabetes and, Alzheimer's disease. The current status of epigenetic research, including the ability to predict disease risk, and key pathophysiological defects are discussed. The significance of defining the contribution of epigenetic defects to nonresolving inflammation and aging, each associated with these diseases, is highlighted, as these are likely to provide new insights into inflammatory disease pathogenesis.

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  • In Alzheimer's disease, changes have been identified in the methylation status of CLU, ABCA7, MS4A6A, and CD2AP, which have been reported to contribute to the development of the disease.

    “On the other hand, in Alzheimer’s disease, for example, changes have been identified in the methylation status of proteins such as human clusterin CLU; ATP binding cassette subfamily A member 7 ABCA7; MS4A6A; and CD2AP, which have been reported to contribute to the development of the disease.”

    From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [86]

    The Alzheimer’s disease > DNA methylation section reports differential methylation in CLU, ABCA7, MS4A6A, and CD2AP and says this indicates an epigenetic contribution to AD susceptibility. It does not establish that methylation changes in those specific genes contribute to disease development; the section says the functional significance of such changes remains to be discovered. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • At the TNF-α locus, epigenetic changes lead to a change in chromatin structure from heterochromatin to euchromatin, and methylation marks are replenished mediated by the MLL enzyme.

    “At its locus, it leads to a change in chromatin structure (from heterochromatin to euchromatin), and methylation marks have also been replenished at this level mediated by the mixed lineage leukemia (MLL) enzyme.”

    From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [86]

    The sections on chromatin architecture and histone modifications (page unavailable) describe chromatin reorganization and methylation marks associated with euchromatin and heterochromatin. They do not establish a heterochromatin-to-euchromatin change at the TNF-α locus or say that MLL replenishes methylation marks there. (LLM, conf=0.78)

    Experimental — accuracy not yet measured

  • Epigenetic mechanisms can mediate the development of chronic inflammation by modulating the expression of molecules such as TNF-α, interleukins, tumor suppressor genes, oncogenes, and the autocrine and paracrine activation of NFK-β.

    “There is evidence to suggest that epigenetic mechanisms can mediate the development of chronic inflammation by modulating the expression of molecules, such as tumor necrosis factor alpha (TNF-α), interleukins, tumor suppressor genes, oncogenes, and the autocrine and paracrine activation of the nuclear factor kappa beta (NFK-β) transcription factor.”

    From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [86]

    The ‘Physiological and pathological inflammation’ and ‘Initiation’ sections say epigenetic changes influence inflammatory pathways and that epigenetic modifiers help regulate inflammatory genes. They also describe cytokine-mediated feed-forward loops. The passages do not support the full specified list of TNF-α, interleukins, tumor suppressor genes and oncogenes, or the asserted autocrine and paracrine activation of NF-κB; searches for those terms did not establish that mechanism. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • miRNAs target the BACE1 protein that regulates the production of amyloid beta platelets, Aβ, which when accumulated contribute to neuroinflammation and progression of Alzheimer's disease.

    “Likewise, it has been reported that there are miRNAs that target the BACE1 protein that regulates the production of amyloid beta platelets, Aβ, which, when accumulated, contribute to the neuroinflammation and progression of this disease [86,87,88].”

    From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [86]

    The Alzheimer’s disease > MicroRNAs section says miRNAs target mRNAs for proteins involved in Aβ processing, including BACE1, which regulates Aβ production. The Molecular and clinical features section says accumulated Aβ plaques contribute to neuroinflammation and disease progression. The citing sentence is imprecise: the paper describes targeting BACE1 mRNA, not the protein directly, and calls the deposits plaques, not platelets. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • Such molecules are constitutively produced by different cells during chronic inflammatory conditions, leading to the development of lung and neurodegenerative diseases and cancer.

    “Such molecules are constitutively produced by different cells during chronic inflammatory conditions, which in turn leads to the development of lung and neurodegenerative diseases and cancer [86].”

    From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [86]

    In “Physiological and pathological inflammation > Initiation” (page not provided), the paper describes cytokine-mediated inflammatory loops involving immune and resident cells. “Alzheimer’s disease > Molecular and clinical features” (page not provided) links failure to resolve brain inflammation with Alzheimer’s pathology. Our copy does not support the stronger claim that these molecules are constitutively produced or that their production leads to lung disease and cancer. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

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Authors
Stylianou, E.
Corresponding author
Stylianou, Eleni
ORCID
Stylianou, Eleni
Venue
Journal of Inflammation Research
Publisher
Informa UK Limited
Published
2018-12
Volume
Volume 12
Pages
1-14
ISSN
1178-7031 (ISSN-L)
DOI
10.2147/jir.s129027
PMC
PMC6304253
OpenAlex
W2903871729
Cited by
79
References
11
Citations by year
2026: 4 · 2025: 8 · 2024: 7 · 2023: 11 · 2022: 17 · 2021: 15 · 2020: 13 · 2019: 4
FWCI
1.35
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Inflammation Research (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
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 › Genetics › Genetic Associations and Epidemiology
Keywords
epigenetics, chronic inflammatory diseases, cardiovascular disease, type 2 diabetes, Alzheimer's disease, nonresolving inflammation, aging, disease risk prediction, inflammatory disease pathogenesis

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