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Metabolic–Epigenetic Interplay in Health and Diseases

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

Deadline for manuscript submissions: 23 October 2026 | Viewed by 925

Special Issue Editor


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Guest Editor
Department of Biosciences, State University of Campinas, Campinas, SP, Brazil
Interests: epigenetics; cell senescence; oral câncer; inflamamtion; cell metabolism

Special Issue Information

Dear Colleagues,

Advances in molecular biology have contributed to the advancement of the understanding of the dynamic crosstalk between cellular metabolism and epigenetic regulation. Metabolites such as acetyl-CoA, NAD+, S-adenosylmethionine, and α-ketoglutarate serve not only as essential intermediates but also as substrates and cofactors for chromatin-modifying enzymes, directly linking metabolic states to gene expression profiles. This metabolic–epigenetic axis plays a pivotal role in maintaining cellular homeostasis and orchestrating adaptive responses to environmental cues. The dysregulation of this interplay has emerged as a critical driver in the pathogenesis of complex diseases, including cancer, neurodegeneration, metabolic syndromes, and aging-related disorders. This Special Issue of the International Journal of Molecular Sciences aims to gather original research and comprehensive reviews that explore the bidirectional relationship between metabolism and epigenetics in both physiological and pathological contexts. We welcome contributions that elucidate novel molecular mechanisms, highlight therapeutic targets, or present integrative omics approaches that expand our understanding of this intricate interface. Through this collection, we seek to advance the field toward innovative strategies for diagnosis, prevention, and treatment based on the metabolic–epigenetic interplay.

Prof. Dr. Ana Paula De Souza
Guest Editor

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Keywords

  • epigenetics
  • metabolism
  • TCA cycle
  • one-carbon cycle
  • aging
  • longevity
  • cancer
  • metabolic syndrome
  • neurodegeneration

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Published Papers (1 paper)

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Research

25 pages, 6947 KB  
Article
Paternal Deprivation Alters Neural Stem Cells Proliferation and Epigenetic Histone Modifications in the Neurogenic Niches of Adult Prairie Voles
by Dulce María Arzate, Guadalupe Denisse Rivera-Bautista, Giovanna Fregoso-Barrera, Analía E. Castro, Francisco Camacho, Daniela Ávila-González, Raúl G. Paredes, Néstor F. Díaz and Wendy Portillo
Int. J. Mol. Sci. 2026, 27(3), 1556; https://doi.org/10.3390/ijms27031556 - 5 Feb 2026
Viewed by 615
Abstract
Paternal deprivation has behavioral, neurochemical, and neuroendocrine consequences in adulthood. Socially monogamous prairie voles (Microtus ochrogaster) raised only by the mother (monoparental care, MP) showed low levels of alloparental behavior and delayed pair bonding formation in adulthood compared to those raised [...] Read more.
Paternal deprivation has behavioral, neurochemical, and neuroendocrine consequences in adulthood. Socially monogamous prairie voles (Microtus ochrogaster) raised only by the mother (monoparental care, MP) showed low levels of alloparental behavior and delayed pair bonding formation in adulthood compared to those raised by both parents (biparental care, BP). However, the effects of paternal deprivation on adult neurogenesis and the epigenetic mechanisms involved remain to be elucidated. Here, we focused on the impact of MP rearing on neural stem cells (NSCs) proliferation under basal conditions and in response to cohabitation with the sexual partner during pair bonding formation. At basal conditions, we found a significant decrease in the number of new proliferative NSCs (BrdU+/SOX2+) in male and female MP voles compared to BP animals in the subventricular (SVZ) and subgranular zone (SGZ). After 24 h of cohabitation, in MP males, there was an increase in the number of newborn cells in the SVZ but not in the SGZ. However, this increased proliferation was lower than in BP males. In females, we did not observe significant differences compared to controls. Finally, we evaluated the enrichment of H3K4me3 (activation) and H3K27me3 (silencing) epigenetic marks in the new cells, finding differences between rearing systems and sexes. Full article
(This article belongs to the Special Issue Metabolic–Epigenetic Interplay in Health and Diseases)
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