Emerging Roles of Epigenetic Regulators in Inflammatory Diseases

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (25 March 2024) | Viewed by 1740

Special Issue Editors


E-Mail Website
Guest Editor
1. State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products, Ningbo University, Ningbo 315211, China
2. Laboratory of Biochemistry and Molecular Biology, School of Marine Sciences, Ningbo University, Ningbo 315211, China
3. Key Laboratory of Applied Marine Biotechnology of Ministry of Education, Ningbo University, Ningbo 315211, China
Interests: drug discovery; inhibitors; epigenetic regulation; protein-protein interaction; metal complex inhibitors; kinase inhibitors; demthylase inhibitors; innate immunity
Special Issues, Collections and Topics in MDPI journals

E-Mail
Guest Editor
College of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530200, China
Interests: anti-tumor discovery and development from Traditional Chinese Medicine; tumor immunology and tumor environment; natural product in senescence treatment
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Emerging evidence suggests that epigenetic events play a crucial role in the initiation and progression of inflammation by influencing various immune components, including cytokines, complements, antimicrobial peptides, cancer-related genes and other inflammation-related genes. These epigenetic modifications can lead to the aberrant activation or suppression of genes in both immune and non-immune cells under inflammatory conditions, contributing to the development of inflammatory diseases such as atherosclerosis, sepsis, diabetes, autoimmune disorders, neurodegenerative diseases and cancer. Although it is well-established that immune responses can induce epigenetic changes during the genesis and progression of inflammatory diseases, the specific contribution of the immune component versus the stimulated host cell in driving these epigenetic modifications remains unclear. Furthermore, while some epigenetic alterations have been extensively characterized, their underlying mechanisms and origins are still not fully understood.

The aim of the Special Issue is to provide a comprehensive overview of the recent advancements and emerging research related to the involvement of epigenetic regulators in various inflammatory diseases and their potential as therapeutic targets. The scope of this Special Issue encompasses, but is not limited to, the following:

(1) Epigenetic modifications in inflammatory disease;
(2) Identification and characterization of epigenetic markers that can serve as diagnostic, prognostic or predictive tools for various diseases;
(3) Novel insights into the development and application of epigenetic-based therapies, including small-molecule inhibitors, epigenetic editing tools and gene-targeting strategies, to modulate aberrant epigenetic regulation in diseases;
(4) Investigation of the underlying molecular mechanisms by which epigenetic regulators, such as DNA methylation, histone modifications, chromatin remodeling and non-coding RNAs, influence gene expression and cellular functions in disease contexts;
(5) Discussions on the translation of epigenetic research findings into clinical applications, including challenges, limitations and future directions for the development of epigenetic-based therapies and personalized medicine approaches.

Through this Special Issue, we aim to provide researchers and clinicians a platform to share cutting-edge research, foster interdisciplinary collaborations and promote a deeper understanding of the emerging roles of epigenetic regulators in inflammatory disease pathogenesis and therapeutic interventions.

You may choose our Joint Special Issue in Biomolecules.

Dr. Guanjun Yang
Dr. Renyikun Yuan
Prof. Dr. Christina Piperi
Guest Editors

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. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • histone modifications
  • microRNAs
  • LncRNAs
  • DNA methylation
  • epigenetic regulation
  • inhibitors or agonists
  • inflammatory diseases

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

13 pages, 2476 KiB  
Article
A High-Fat and High-Fructose Diet Exacerbates Liver Dysfunction by Regulating Sirtuins in a Murine Model
by Zehuan Ding, Jian Zhang and Mahua Choudhury
Life 2024, 14(6), 729; https://doi.org/10.3390/life14060729 - 5 Jun 2024
Cited by 1 | Viewed by 1317
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is rapidly emerging as the most prevalent chronic liver disease, closely linked to the escalating rates of diabesity. The Western diet’s abundance of fat and fructose significantly contributes to MASLD, disrupting hepatic glucose metabolism. We previously demonstrated [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is rapidly emerging as the most prevalent chronic liver disease, closely linked to the escalating rates of diabesity. The Western diet’s abundance of fat and fructose significantly contributes to MASLD, disrupting hepatic glucose metabolism. We previously demonstrated that a high-fat and high-fructose diet (HFHFD) led to increased body and liver weight compared to the low-fat diet (LFD) group, accompanied by glucose intolerance and liver abnormalities, indicating an intermediate state between fatty liver and liver fibrosis in the HFHFD group. Sirtuins are crucial epigenetic regulators associated with energy homeostasis and play a pivotal role in these hepatic dysregulations. Our investigation revealed that HFHFD significantly decreased Sirt1 and Sirt7 gene and protein expression levels, while other sirtuins remained unchanged. Additionally, glucose 6-phosphatase (G6Pase) gene expression was reduced in the HFHFD group, suggesting a potential pathway contributing to fibrosis progression. Chromatin immunoprecipitation analysis demonstrated a significant increase in histone H3 lysine 18 acetylation within the G6Pase promoter in HFHFD livers, potentially inhibiting G6Pase transcription. In summary, HFHFD may inhibit liver gluconeogenesis, potentially promoting liver fibrosis by regulating Sirt7 expression. This study offers an epigenetic perspective on the detrimental impact of fructose on MASLD progression. Full article
(This article belongs to the Special Issue Emerging Roles of Epigenetic Regulators in Inflammatory Diseases)
Show Figures

Figure 1

Back to TopTop