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Epigenetic Mechanisms and Inflammatory Response in Endocrine Disorders
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Epigenetic Mechanisms and Inflammatory Response in Endocrine Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 18047

Special Issue Editor

Prof. Dr. Dariusz Szukiewicz

E-Mail Website
Guest Editor
Department of Biophysics, Physiology and Pathophysiology, Faculty of Health Sciences, Medical University of Warsaw, Chalubinskiego 5 (4th Floor), 02-004 Warsaw, Poland
Interests: inflammation; cytokine network; human placenta; stem cells in reproductive tissues; pathophysiology of diabetes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epigenetics deals with heritable phenotype changes under the influence of environmental factors that do not involve alterations in the DNA sequence. These changes are achieved through epigenetic mechanisms involving DNA methylation and hydroxymethylation, histone post-translational modifications, remodeling and repositioning of nucleosomes, higher-order chromatin structure reorganization, non-coding RNA regulation, and RNA modifications. Naturally, these epigenetic events may modulate the activity of both inflammatory and anti-inflammatory genes and have been identified as central pathophysiological factors in addition to genetic disease predisposition and as co-factors determining the course of inflammatory response. Interactions of the endocrine system with inflammation, including autoimmune and autoinflammatory diseases, are very common. The endocrine and immune system crosstalk and multiple immune processes are involved in endocrine diseases. Hormonal imbalances can increase inflammation, which in turn can further disrupt hormone production. For example, insulin resistance has been recognized as an inflammatory state with increased concentrations of inflammatory markers.

This Special Issue is dedicated to all aspects of epigenetic regulation of the inflammatory response in endocrine disorders. When considering your submission, please keep in mind that IJMS is a journal of molecular science. However, submissions of clinical studies with biomolecular experiments or pathological research with case sample data are welcomed.

Prof. Dr. Dariusz Szukiewicz
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • epigenetic mechanisms
  • epigenetic regulation
  • inflammation
  • inflammatory response
  • endocrine disorders
  • autoimmune endocrine diseases
  • hormonal imbalances
  • obesity-induced inflammation

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Published Papers (3 papers)

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Research

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11 pages, 1032 KiB  
Communication
SERPINE1 DNA Methylation Levels Quantified in Blood Cells at Five Years of Age Are Associated with Adiposity and Plasma PAI-1 Levels at Five Years of Age
by Amelie Taschereau, Véronique Desgagné, Sabrina Faleschini, Renée Guérin, Catherine Allard, Patrice Perron, Marie-France Hivert and Luigi Bouchard
Int. J. Mol. Sci. 2022, 23(19), 11833; https://doi.org/10.3390/ijms231911833 - 5 Oct 2022
Cited by 1 | Viewed by 1979
Abstract
Plasminogen activator inhibitor (PAI-1) expression has been associated with a higher risk of development of obesity. DNA methylation (DNAm) is an epigenetic mechanism regulating gene transcription and likely involved in the fetal programming of childhood obesity. Our study aimed to assess the associations [...] Read more.
Plasminogen activator inhibitor (PAI-1) expression has been associated with a higher risk of development of obesity. DNA methylation (DNAm) is an epigenetic mechanism regulating gene transcription and likely involved in the fetal programming of childhood obesity. Our study aimed to assess the associations between PAI-1 gene (SERPINE1) DNAm, plasma PAI-1 levels, and adiposity at five years of age. We analyzed DNAm and anthropometric data from 146 girls and 177 boys from the Gen3G prospective birth cohort. We assessed adiposity using BMI z-scores, waist circumference, total skinfolds, and percentages of total, android, and trunk fat measured by dual-energy radiography (DXA). We estimated blood cell DNAm levels at 15 CpG sites within SERPINE1 using the methylationEPIC array. After correction for multiple testing, we found that lower DNAm in SERPINE1 intron 3 (cg11353706) was associated with greater adiposity levels in girls (waist circumference: r = −0.258, p = 0.002; skinfolds: r = −0.212, p = 0. 013; android fat: r = −0.215, p = 0.015; BMI z-score: r = −0.278, p < 0.001) and that lower DNAm in the SERPINE1 promoter (cg19722814) was associated with higher plasma PAI-1 levels in boys (r = −0.178, p = 0.021). Our study suggests that DNAm levels at the SERPINE1 gene locus are negatively correlated with adiposity, but not with plasma PAI-1 levels, in young girls only. Full article
(This article belongs to the Special Issue Epigenetic Mechanisms and Inflammatory Response in Endocrine Disorders)
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Review

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27 pages, 2526 KiB  
Review
Modulation of the Inflammatory Response in Polycystic Ovary Syndrome (PCOS)—Searching for Epigenetic Factors
by Dariusz Szukiewicz, Seweryn Trojanowski, Anna Kociszewska and Grzegorz Szewczyk
Int. J. Mol. Sci. 2022, 23(23), 14663; https://doi.org/10.3390/ijms232314663 - 24 Nov 2022
Cited by 23 | Viewed by 7664
Abstract
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. Despite its incidence, the syndrome is poorly understood and remains underdiagnosed, and female patients are diagnosed with a delay. The heterogenous nature of this complex disorder results from [...] Read more.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. Despite its incidence, the syndrome is poorly understood and remains underdiagnosed, and female patients are diagnosed with a delay. The heterogenous nature of this complex disorder results from the combined occurrence of genetic, environmental, endocrine, and behavioral factors. Primary clinical manifestations of PCOS are derived from the excess of androgens (anovulation, polycystic ovary morphology, lack of or scanty, irregular menstrual periods, acne and hirsutism), whereas the secondary manifestations include multiple metabolic, cardiovascular, and psychological disorders. Dietary and lifestyle factors play important roles in the development and course of PCOS, which suggests strong epigenetic and environmental influences. Many studies have shown a strong association between PCOS and chronic, low-grade inflammation both in the ovarian tissue and throughout the body. In the vast majority of PCOS patients, elevated values of inflammatory markers or their gene markers have been reported. Development of the vicious cycle of the chronic inflammatory state in PCOS is additionally stimulated by hyperinsulinemia and obesity. Changes in DNA methylation, histone acetylation and noncoding RNA levels are presented in this review in the context of oxidative stress, reactive oxygen species, and inflammatory signaling in PCOS. Epigenetic modulation of androgenic activity in response to inflammatory signaling is also discussed. Full article
(This article belongs to the Special Issue Epigenetic Mechanisms and Inflammatory Response in Endocrine Disorders)
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13 pages, 954 KiB  
Review
Ketone Bodies as Metabolites and Signalling Molecules at the Crossroad between Inflammation and Epigenetic Control of Cardiometabolic Disorders
by Nadia Bendridi, Anna Selmi, Aneta Balcerczyk and Luciano Pirola
Int. J. Mol. Sci. 2022, 23(23), 14564; https://doi.org/10.3390/ijms232314564 - 23 Nov 2022
Cited by 15 | Viewed by 7617
Abstract
For many years, it has been clear that a Western diet rich in saturated fats and sugars promotes an inflammatory environment predisposing a person to chronic cardiometabolic diseases. In parallel, the emergence of ketogenic diets, deprived of carbohydrates and promoting the synthesis of [...] Read more.
For many years, it has been clear that a Western diet rich in saturated fats and sugars promotes an inflammatory environment predisposing a person to chronic cardiometabolic diseases. In parallel, the emergence of ketogenic diets, deprived of carbohydrates and promoting the synthesis of ketone bodies imitating the metabolic effects of fasting, has been shown to provide a possible nutritional solution to alleviating diseases triggered by an inflammatory environment. The main ketone body, β-hydroxybutyrate (BHB), acts as an alternative fuel, and also as a substrate for a novel histone post-translational modification, β-hydroxybutyrylation. β-hydroxybutyrylation influences the state of chromatin architecture and promotes the transcription of multiple genes. BHB has also been shown to modulate inflammation in chronic diseases. In this review, we discuss, in the pathological context of cardiovascular risks, the current understanding of how ketone bodies, or a ketogenic diet, are able to modulate, trigger, or inhibit inflammation and how the epigenome and chromatin remodeling may be a key contributor. Full article
(This article belongs to the Special Issue Epigenetic Mechanisms and Inflammatory Response in Endocrine Disorders)
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