Epigenetic and Metabolic Control of Neural Development, Injury and Repair

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About this Research Topic

Submission deadlines

  1. Manuscript Submission Deadline 20 March 2027

  2. This Research Topic is currently accepting articles

Background

The development and regeneration of the mammalian nervous system represent one of the most complex biological processes, requiring the finely tuned coordination of neural stem and progenitor cell proliferation, differentiation, and migration. Emerging evidence demonstrates that these events are not solely governed by intrinsic genetic programs but also depend on the dynamic interplay between metabolic states and epigenetic modifications. Recent studies reveal that metabolites can directly influence the availability and activity of epigenetic enzymes, while chromatin remodeling can reciprocally alter cellular metabolic fluxes. Despite remarkable progress, critical gaps persist in understanding how these bidirectional interactions shape neural cell fate decisions during brain development, as well as their roles in neurodevelopmental disorders and central nervous system (CNS) injury responses. Key unresolved issues include identifying the precise molecular nodes that integrate metabolic and epigenetic signals during cortical expansion and determining how their dysregulation contributes to disease pathogenesis.

This Research Topic aims to explore the interdependence between metabolic pathways and epigenetic mechanisms in neural development, maintenance, and regeneration. By fostering the integration of multi-omics datasets, functional studies, and innovative imaging or lineage-tracing approaches, the objective is to define how metabolic cues contribute to epigenetic reprogramming and how these processes collectively influence neurogenesis and repair. Specifically, it seeks to uncover novel mechanisms by which metabolic intermediates govern chromatin states, identify master regulators of neuroepigenetic balance, and evaluate therapeutic potential in modulating these pathways for neural repair and regeneration. This Research Topic therefore encourages interdisciplinary research that bridges molecular neurobiology, epigenomics, and cellular metabolism to illuminate new strategies for restoring CNS function after injury or in disease.

To gather further insights into the reciprocal regulation between metabolism and epigenetics during neural development and regeneration, we welcome articles addressing, but not limited to, the following themes:

o Epigenetic regulation in neural cell fate: DNA methylation, histone modifications, and non-coding RNAs in neurogenesis and gliogenesis.

o Metabolic reprogramming in the brain: how glycolytic, lipid, and mitochondrial pathways influence progenitor dynamics and cortical expansion.

o Crosstalk between metabolism and epigenetics: metabolites as substrates or cofactors modulating chromatin enzymes.

o Signaling networks integrating metabolic and epigenetic control: pathways such as YAP/TAZ, SHH, or kinase cascades in neural tissue growth.

o Single-cell and spatial multi-omics: mapping developmental and injury-related trajectories using high-resolution techniques.

o Nerve injury and regeneration: epigenetic and metabolic mechanisms underlying axonal regeneration, glial scar remodeling, and functional recovery.

o Neurodevelopmental disorders: dysfunctional metabolic-epigenetic networks in neuropsychiatric or neurodevelopmental disease contexts.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

  • Brief Research Report
  • Data Report
  • Editorial
  • FAIR² Data
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review
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Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Keywords: Neural Development, Epigenetics, Cell Metabolism, Nerve Injury and Repair, Single-cell Multi-omics, Cortical Expansion, Cell Fate Determination

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