Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Molecular Research and Therapeutic Targets in Acute Settings: Ischemic and...
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Molecular Research and Therapeutic Targets in Acute Settings: Ischemic and Traumatic Brain Injuries

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

Deadline for manuscript submissions: 20 January 2025 | Viewed by 2468

Special Issue Editor

Dr. Hylde Zirpoli

E-Mail Website
Guest Editor
Department of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA
Interests: cute hypoxic-ischemic injuries

Special Issue Information

Dear Colleagues,

The pathophysiology of cerebral ischemia and brain trauma indicates that similar mechanisms contribute to the loss of cellular integrity and tissue damage.

Brain injuries result from the complex interplay of multiple pathways including excitotoxicity, ionic imbalance, oxidative/nitrative stress and blood–brain barrier (BBB) disruption. With cell type-specific pathomechanisms, acute cerebral insults activate neuronal cell death, inflammation from microglia activation and immune cell infiltration, accompanied with astrogliosis, and complex glia–neuron exchanges, and they are important elements in the pathological onset and the progression of ischemic or trauma-triggered brain damage.

From exploring these molecular mechanisms and dissecting the role of specific cell-type signaling pathways or cell–cell interactions, each contribution will aim to provide insights that pave the way for more effective therapeutic approaches.

I look forward to receiving your contributions.

Dr. Hylde Zirpoli
Guest Editor

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. 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

  • ischemic brain injury
  • traumatic brain insult
  • cell-type specific molecular mechanisms
  • therapy
  • target discovery
  • repurposing
  • efficacy studies
  • new drug formulations
  • high-throughput technologies
  • proteomics
  • metabolomics
  • microarray
  • next-generation sequencing
  • BBB disruption
  • gliosis
  • neuronal loss
  • neurobehavior
  • age-related molecular mechanisms in brain injury

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 (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

22 pages, 12635 KiB  
Article
Neuroprotective Effect of Clemastine Improved Oligodendrocyte Proliferation through the MAPK/ERK Pathway in a Neonatal Hypoxia Ischemia Rat Model
by Maria E. Bernis, Charlotte Hakvoort, Efe Nacarkucuk, Hannah Burkard, Anna-Sophie Bremer, Margit Zweyer, Elke Maes, Kora A. Grzelak and Hemmen Sabir
Int. J. Mol. Sci. 2024, 25(15), 8204; https://doi.org/10.3390/ijms25158204 - 27 Jul 2024
Viewed by 634
Abstract
Neonatal hypoxic-ischemic encephalopathy is the most common cause of long-term disability in term neonates, and white matter injury is the primary cause of cerebral palsy. Therapies that focus on the neuroprotection of myelination and oligodendrocyte proliferation could potentially ameliorate long-lasting neurological impairments after [...] Read more.
Neonatal hypoxic-ischemic encephalopathy is the most common cause of long-term disability in term neonates, and white matter injury is the primary cause of cerebral palsy. Therapies that focus on the neuroprotection of myelination and oligodendrocyte proliferation could potentially ameliorate long-lasting neurological impairments after hypoxic-ischemic encephalopathy. Clemastine, a histamine H1 antagonist, has been shown to exert neuroprotective effects in multiple sclerosis and spinal cord injury by promoting oligodendrogenesis and re-myelination. In this study, we demonstrated the neuroprotective effects of clemastine in our rat model of neonatal hypoxic-ischemic brain injury. Animals received a single intraperitoneal injection of either vehicle or clemastine (10 mg/kg) for 6 consecutive days. Our results showed a significant reduction in white matter loss after treatment, with a clear effect of clemastine on oligodendrocytes, showing a significant increase in the number of Olig2+ cells. We characterized the MAPK/ERK pathway as a potential mechanistic pathway underlying the neuroprotective effects of clemastine. Altogether, our results demonstrate that clemastine is a potential compound for the treatment of hypoxic-ischemic encephalopathy, with a clear neuroprotective effect on white matter injury by promoting oligodendrogenesis. Full article
(This article belongs to the Special Issue Molecular Research and Therapeutic Targets in Acute Settings: Ischemic and Traumatic Brain Injuries)
►▼ Show Figures

Figure 1

20 pages, 18479 KiB  
Article
Pulmonary Effects of Traumatic Brain Injury in Mice: A Gene Set Enrichment Analysis
by Wei-Hung Chan, Shih-Ming Huang and Yi-Lin Chiu
Int. J. Mol. Sci. 2024, 25(5), 3018; https://doi.org/10.3390/ijms25053018 - 5 Mar 2024
Viewed by 1393
Abstract
Acute lung injury occurs in 20–25% of cases following traumatic brain injury (TBI). We investigated changes in lung transcriptome expression post-TBI using animal models and bioinformatics. Employing unilateral controlled cortical impact for TBI, we conducted microarray analysis after lung acquisition, followed by gene [...] Read more.
Acute lung injury occurs in 20–25% of cases following traumatic brain injury (TBI). We investigated changes in lung transcriptome expression post-TBI using animal models and bioinformatics. Employing unilateral controlled cortical impact for TBI, we conducted microarray analysis after lung acquisition, followed by gene set enrichment analysis of differentially expressed genes. Our findings indicate significant upregulation of inflammation-related genes and downregulation of nervous system genes. There was enhanced infiltration of adaptive immune cells, evidenced by positive enrichment in Lung-Th1, CD4, and CD8 T cells. Analysis using the Tabula Sapiens database revealed enrichment in lung-adventitial cells, pericytes, myofibroblasts, and fibroblasts, indicating potential effects on lung vasculature and fibrosis. Gene set enrichment analysis linked TBI to lung diseases, notably idiopathic pulmonary hypertension. A Venn diagram overlap analysis identified a common set of 20 genes, with FOSL2 showing the most significant fold change. Additionally, we observed a significant increase in ADRA1A→IL6 production post-TBI using the L1000 library. Our study highlights the impact of brain trauma on lung injury, revealing crucial gene expression changes related to immune cell infiltration, cytokine production, and potential alterations in lung vasculature and fibrosis, along with a specific spectrum of disease influence. Full article
(This article belongs to the Special Issue Molecular Research and Therapeutic Targets in Acute Settings: Ischemic and Traumatic Brain Injuries)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop