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The Cellular and Molecular Mechanisms of Central Nervous System Injury
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The Cellular and Molecular Mechanisms of Central Nervous System Injury

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: 20 August 2026 | Viewed by 1553

Special Issue Editors

Dr. Laurent R. Gauthier

E-Mail Website
Guest Editor
1. Université Paris Cité, Inserm, CEA, Stabilité Génétique Cellules Souches et Radiations, LRP/iRCM/IBFJ, F-92265 Fontenay-aux-Roses, France
2. Université Paris-Saclay, Inserm, CEA, Stabilité Génétique Cellules Souches et Radiations, LRP/iRCM/IBFJ, F-92265 Fontenay-aux-Roses, France
Interests: glioma stem cells; cell migration; cell invasion; ionizing radiation; DNA repair; telomere; videomicroscopy; neural stem cells
Dr. José R. Pineda

E-Mail Website
Guest Editor
Cell Signaling Lab, Department of Cell Biology and Histology, Faculty of Medicine and Nursery, University of the Basque Country (UPV/EHU), Bilbao, Spain
Interests: cancer stem cells; glioma; glioma stem cells; neural stem cells; dental pulp stem cells; cell therapy; niche environment; scaffolds; neurogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue of the International Journal of Molecular Sciences highlights recent advances in elucidating the cellular and molecular mechanisms underlying injury to the central nervous system (CNS). CNS damage can result from diverse etiologies, including trauma, ischemia, inflammation, neoplasms, infections, and exposure to external agents such as radiation, chemotherapeutic drugs, or environmental toxins. These insults often lead to persistent neurological dysfunction and limited regenerative capacity, underscoring the urgent need to understand the fundamental biological processes involved for developing effective treatments.

We welcome original research articles, reviews, and perspectives that investigate key mechanisms such as oxidative stress, DNA damage responses, inflammation, apoptosis, neuroregeneration, blood–brain barrier disruption, and altered intercellular communication. Submissions employing in vitro systems, animal models, or patient-derived approaches—including brain organoids, advanced imaging, and high-throughput omics—are particularly encouraged. By integrating multidisciplinary approaches, this Special Issue aims to provide a comprehensive overview of CNS injury and foster the development of innovative diagnostic and therapeutic strategies.

Dr. Laurent R. Gauthier
Dr. José R. Pineda
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 250 words) can be sent to the Editorial Office for assessment.

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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • central nervous system damage
  • CNS
  • oxidative stress
  • DNA damage responses
  • neuroregeneration
  • blood–brain barrier disruption

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Published Papers (2 papers)

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Research

35 pages, 9030 KB  
Article
Multimodal Single-Cell Transcriptomic and Chromatin Accessibility Profiling Reveals Monocyte-Derived Macrophage Dynamics Following Ischemic Stroke
by Milton H. Hamblin, Rabi Murad, Austin C. Boese, Huijie Huang, Rebecca A. Porritt, Tanvi Bobba and Jean-Pyo Lee
Int. J. Mol. Sci. 2026, 27(8), 3657; https://doi.org/10.3390/ijms27083657 - 20 Apr 2026
Viewed by 607
Abstract
Ischemic stroke promotes monocyte recruitment to the injured brain and their differentiation into monocyte-derived macrophages (MDMs). These cells contribute to debris clearance but may also exacerbate neuroinflammation. However, the heterogeneity of MDM subsets and the phenotypic transitions that shape MDM functional states during [...] Read more.
Ischemic stroke promotes monocyte recruitment to the injured brain and their differentiation into monocyte-derived macrophages (MDMs). These cells contribute to debris clearance but may also exacerbate neuroinflammation. However, the heterogeneity of MDM subsets and the phenotypic transitions that shape MDM functional states during the subacute phase of stroke remain incompletely characterized. To address this, we first performed single-cell RNA sequencing (scRNA-seq) to define the transcriptional landscape of the mouse brain 48 h after transient middle cerebral artery occlusion/reperfusion compared with sham controls. Reclustering of macrophage-lineage cells identified multiple MDM subsets, including a distinct Cd68hi/Ctsdhi MDM subset enriched for lysosomal and lipid-processing gene expression programs. Cell trajectory inference supported a transition from early recruited MDMs toward the Cd68hi/Ctsdhi state, accompanied by induction of transcriptomic networks that drive MDM function to favor a clearance-competent phenotype in response to ischemic stroke. Complementary single-cell ATAC sequencing (scATAC-seq) demonstrated cell type-specific chromatin remodeling after stroke and revealed MDM subclusters with accessibility at key loci regulating lysosomal function and lipid metabolism. Together, our findings define a cellular and regulatory framework of the subacute post-stroke brain and identify a lysosome-enriched Cd68hi/Ctsdhi MDM trajectory, highlighting endolysosomal and lipid-processing programs during early stroke recovery. Full article
(This article belongs to the Special Issue The Cellular and Molecular Mechanisms of Central Nervous System Injury)
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26 pages, 6660 KB  
Article
Kaempferol Protects Against Amyloid β Overproduction and the Rise of Phospho-Tau 217 and Phospho-Tau 181 in the Rat Cerebellum Induced by Acute 3-Nitropropionic Acid Administration
by Virginio García-López, Carmen López-Sánchez, Joana Poejo, Ricardo Lagoa, Dorinda Marques-da-Silva, Virginio García-Martínez and Carlos Gutierrez-Merino
Int. J. Mol. Sci. 2026, 27(6), 2880; https://doi.org/10.3390/ijms27062880 - 22 Mar 2026
Viewed by 518
Abstract
The 3-nitropropionic acid (NPA) promotes neurological alterations in the striatum, hippocampus and vicinal motor and pre-motor cortical areas, and in the cerebellum. The neurological alterations induced by systemic NPA administration resemble those found in Huntington’s disease. In previous works, we have [...] Read more.
The 3-nitropropionic acid (NPA) promotes neurological alterations in the striatum, hippocampus and vicinal motor and pre-motor cortical areas, and in the cerebellum. The neurological alterations induced by systemic NPA administration resemble those found in Huntington’s disease. In previous works, we have shown that intraperitoneal (i.p.) administration of kaempferol can efficiently protect against striatum degeneration and against motor neurological dysfunctions induced by NPA. In this work, we show that i.p. administration of kaempferol also protects against the increase in pro-inflammatory cytokines that potentiate the activation of complement C3 protein (a biomarker of A1-type reactive astrocytes generation) and overproduction of neurotoxic amyloid β (Aβ) peptides in the cerebellum of rats treated with acute i.p. administration of NPA. In NPA-treated rats, large multipolar neurons of cerebellar nuclei and Purkinje neurons of the cerebellar cortex are the cells that are most intensely stained by anti-C3 and by anti-Aβ antibodies. In addition, we found that kaempferol also protects against the NPA-induced increase in phospho-tau 217 and phospho-tau 181 in the cerebellum, and our results pointed out that the NPA-induced phospho-tau 217 colocalizes with Aβ(1-42) more closely than phospho-tau 181, both in dentate nucleus and cerebellar cortex. Also, our results unveil another novel brain-protective action of i.p. kaempferol co-administration: namely, its ability to prevent microhemorrhages induced in the cerebellar nuclei area by acute NPA administration. In conclusion, the results of this work show a potent protection of kaempferol against the NPA-induced increase in degeneration biomarkers in the cerebellum. Full article
(This article belongs to the Special Issue The Cellular and Molecular Mechanisms of Central Nervous System Injury)
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