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Biomolecules
Special Issues
Metabolic Regulation of Brain Diseases: A Focus on Epigenetic Mechanisms
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Metabolic Regulation of Brain Diseases: A Focus on Epigenetic Mechanisms

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 5930

Special Issue Editors

Dr. Simona Daniele

E-Mail Website
Guest Editor
Department of Pharmacy, University of Pisa, Via Bonanno 6, 56126 Pisa, Italy
Interests: intracellular pathways; molecular signaling; epigenetic regulation; brain diseases; neurodegeneration; glioblastoma multiforme
Special Issues, Collections and Topics in MDPI journals
Dr. Sara Carpi

E-Mail Website
Guest Editor
Department of Pharmacy, University of Pisa, via Bonanno 6, 56126 Pisa, Italy
Interests: microRNA; natural compound; nutraceutical; Krabbe disease

Special Issue Information

Dear Colleagues, 

Brain diseases affect the lives of 1 in 6 people and are considered as a significant global healthcare problem. Recently, progress from different sides has been made and researchers have shown that metabolic alterations seem to be a key event in brain disease induction and progression. Others have shown that metabolic disfunction involves changes in chromatin and chromatin-modifying enzymes, which can contribute to a persistent dysregulated metabolic phenotype. Indeed, a rising number of studies link epigenetic alterations with metabolic alterations in brain diseases.

Epigenetics and metabolism trade interacting factors dynamically and reciprocally, while constantly being modulated by multifactorial external stimuli, unfolding correlations among different brain pathological conditions.

The aim of this Special Issue is to gather research papers and reviews focused on the epigenetic mechanisms involved in the regulation of the metabolism in brain pathologic conditions, including neurodegenerative diseases and brain tumors. Papers that will get new insights into the molecular pathways and potential new therapeutic approaches will be appreciated.

Dr. Simona Daniele
Dr. Sara Carpi
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. Biomolecules 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 2700 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

  • brain diseases
  • epigenetics
  • metabolism
  • Central Nervous System (CNS)
  • cellular neuroenergetics

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Published Papers (2 papers)

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Research

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14 pages, 1836 KiB  
Article
6-Hydroxydopamine Induces Abnormal Iron Sequestration in BV2 Microglia by Activating Iron Regulatory Protein 1 and Inhibiting Hepcidin Release
by Manman Xu, Yinghui Li, Dapeng Meng, Danyang Zhang, Bingjing Wang, Junxia Xie and Jun Wang
Biomolecules 2022, 12(2), 266; https://doi.org/10.3390/biom12020266 - 7 Feb 2022
Cited by 14 | Viewed by 2556
Abstract
Disrupted iron homeostasis in the substantia nigra pars compacta (SNpc) is an important pathological mechanism in Parkinson’s disease (PD). It is unclear what role microglia play in iron metabolism and selective iron deposition in the SNpc of PD brain. In this study, we [...] Read more.
Disrupted iron homeostasis in the substantia nigra pars compacta (SNpc) is an important pathological mechanism in Parkinson’s disease (PD). It is unclear what role microglia play in iron metabolism and selective iron deposition in the SNpc of PD brain. In this study, we observed that 6-hydroxydopamine (6-OHDA) induced the expression of divalent metal transporter-1 (DMT1) and iron influx in BV2 microglia cells, which might be associated with the upregulation of iron regulatory protein 1 (IRP1) expression. Moreover, we found that 6-OHDA had no significant effect on the expression of ferroportin 1 (FPN1) and iron efflux in BV2 microglial cells, which might be the combined action of IRP1 upregulation and reduced hepcidin levels. Furthermore, 6-OHDA treatment activated BV2 microglia and enhanced the release of pro-inflammatory cytokines. Interestingly, iron overloading suppressed IRP1 expression, thus downregulating DMT1 and upregulating FPN1 levels in these microglial cells. On the contrary, iron deficiency activated IRP1, leading to increased expression of DMT1 and decreased expression of FPN1—which indicates that activated IRP1 induces iron overloading in 6-OHDA-treated microglia, but not iron overloading modulates the expression of IRP1. Taken together, our data suggest that 6-OHDA can regulate the expression of DMT1 and FPN1 by activating IRP1 and inhibiting hepcidin release, thus leading to abnormal iron sequestration in microglia. In addition, 6-OHDA can activate microglia, which leads to increased release of pro-inflammatory factors that can further induce genome damage in dopaminergic neurons. Full article
(This article belongs to the Special Issue Metabolic Regulation of Brain Diseases: A Focus on Epigenetic Mechanisms)
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Review

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12 pages, 303 KiB  
Review
BXD Recombinant Inbred Mice as a Model to Study Neurotoxicity
by Airton C. Martins, Caridad López-Granero, Beatriz Ferrer, Alexey A. Tinkov, Anatoly V. Skalny, Monica M. B. Paoliello and Michael Aschner
Biomolecules 2021, 11(12), 1762; https://doi.org/10.3390/biom11121762 - 25 Nov 2021
Cited by 7 | Viewed by 2649
Abstract
BXD recombinant inbred (RI) lines represent a genetic reference population derived from a cross between C57BL/6J mice (B6) and DBA/2J mice (D2), which through meiotic recombination events possesses recombinant chromosomes containing B6 or D2 haplotype segments. The quantitative trait loci (QTLs) are the [...] Read more.
BXD recombinant inbred (RI) lines represent a genetic reference population derived from a cross between C57BL/6J mice (B6) and DBA/2J mice (D2), which through meiotic recombination events possesses recombinant chromosomes containing B6 or D2 haplotype segments. The quantitative trait loci (QTLs) are the locations of segregating genetic polymorphisms and are fundamental to understanding genetic diversity in human disease susceptibility and severity. QTL mapping represents the typical approach for identifying naturally occurring polymorphisms that influence complex phenotypes. In this process, genotypic values at markers of known genomic locations are associated with phenotypic values measured in a segregating population. Indeed, BXD RI strains provide a powerful tool to study neurotoxicity induced by different substances. In this review, we describe the use of BXD RI lines to understand the underlying mechanisms of neurotoxicity in response to ethanol and cocaine, as well as metals and pesticide exposures. Full article
(This article belongs to the Special Issue Metabolic Regulation of Brain Diseases: A Focus on Epigenetic Mechanisms)
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