ijms-logo

Journal Browser

Journal Browser

Molecular Mechanisms and Pathophysiology of Acute Stroke 2.0

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: closed (30 November 2023) | Viewed by 4750

Special Issue Editors


E-Mail Website
Guest Editor
Unit of Cerebrovascular Diseases, Service of Neurology, Hospital Universitari del Sagrat Cor, Universitat de Barcelona, Barcelona, Catalonia, Spain
Interests: cerebrovascular diseases; lacunar strokes; acute stroke; vascular cognitive impairment
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Cellular and Molecular Neurobiology Research Group, Department of Neurosciences, Germans Trias i Pujol Research Institute (IGTP), 08916 Badalona, Spain
Interests: stroke; iron dyshomeostasis; excitotoxicity; ferroptosis; new-generation therapies; glutamate excitotoxicity; transferrin; free radicals; therapeutic targets; proteomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Stroke remains a leading cause of death and disability, and has a complex pathophysiology. Increasing evidence suggests that the brain is exquisitely sensitive to even short-duration ischemia, and that multiple mechanisms are involved in the tissue damage that results from cerebral ischemia. Ischemic stroke initiates a cascade of events, including ATP depletion, ionic dysregulation, the increased release of glutamate, the excess production of free radicals, and edema as well as inflammation; all of these events eventually contribute to cell death. In contrast, in an intracerebral hemorrhage, the oppression and destruction of brain tissue by a hematoma are the primary causes of brain injury, but the inflammation, coagulation response, and toxicity of the released hemoglobin play pivotal roles as well. Cell death after stroke has been attributed in the past mainly to necrosis or apoptosis, but recent reports show the involvement of other newly described forms of cell death.

The goal of this Special Issue is to provide a critical overview of the underlying factors involved in stroke-related brain injury, especially the role of cell signaling in excitotoxicity, inflammation, apoptosis, and the newly described types of cell death, such as ferroptosis. Gene and protein expression profiles after stroke in addition to neurogenesis, angiogenesis, and neuroplasticity are other important features in stroke, and should lead to a better understanding of the pathophysiology of acute stroke.

We warmly welcome submissions, including original articles and reviews, on these hot topics.

Dr. Adria Arboix
Dr. Teresa Gasull
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. 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

  • stroke
  • ischemic
  • hemorrhagic
  • neuronal death
  • molecular mechanisms
  • inflammation
  • epigenetics
  • ischemic tolerance
  • ferroptosis
  • free radicals

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)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

16 pages, 16447 KiB  
Article
Re-Evaluating the Relevance of the Oxygen–Glucose Deprivation Model in Ischemic Stroke: The Example of Cdk Inhibition
by Tine D’aes, Quentin Marlier, Sébastien Verteneuil, Pascale Quatresooz, Renaud Vandenbosch and Brigitte Malgrange
Int. J. Mol. Sci. 2023, 24(8), 7009; https://doi.org/10.3390/ijms24087009 - 10 Apr 2023
Cited by 3 | Viewed by 2393
Abstract
Previous research has shown that cyclin-dependent kinases (Cdks) that play physiological roles in cell cycle regulation become activated in post-mitotic neurons after ischemic stroke, resulting in apoptotic neuronal death. In this article, we report our results using the widely used oxygen–glucose deprivation (OGD) [...] Read more.
Previous research has shown that cyclin-dependent kinases (Cdks) that play physiological roles in cell cycle regulation become activated in post-mitotic neurons after ischemic stroke, resulting in apoptotic neuronal death. In this article, we report our results using the widely used oxygen–glucose deprivation (OGD) in vitro model of ischemic stroke on primary mouse cortical neurons to investigate whether Cdk7, as part of the Cdk-activating kinase (CAK) complex that activates cell cycle Cdks, might be a regulator of ischemic neuronal death and may potentially constitute a therapeutic target for neuroprotection. We found no evidence of neuroprotection with either pharmacological or genetic invalidation of Cdk7. Despite the well-established idea that apoptosis contributes to cell death in the ischemic penumbra, we also found no evidence of apoptosis in the OGD model. This could explain the absence of neuroprotection following Cdk7 invalidation in this model. Neurons exposed to OGD seem predisposed to die in an NMDA receptor-dependent manner that could not be prevented further downstream. Given the direct exposure of neurons to anoxia or severe hypoxia, it is questionable how relevant OGD is for modeling the ischemic penumbra. Due to remaining uncertainties about cell death after OGD, caution is warranted when using this in vitro model to identify new stroke therapies. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Acute Stroke 2.0)
Show Figures

Figure 1

Review

Jump to: Research

25 pages, 1033 KiB  
Review
The Role of Epigenetics in Brain Aneurysm and Subarachnoid Hemorrhage: A Comprehensive Review
by Isabel Fernández-Pérez, Adrià Macias-Gómez, Antoni Suárez-Pérez, Marta Vallverdú-Prats, Eva Giralt-Steinhauer, Lidia Bojtos, Sílvia Susin-Calle, Ana Rodriguez-Campello, Daniel Guisado-Alonso, Joan Jimenez-Balado, Jordi Jiménez-Conde and Elisa Cuadrado-Godia
Int. J. Mol. Sci. 2024, 25(6), 3433; https://doi.org/10.3390/ijms25063433 - 19 Mar 2024
Cited by 2 | Viewed by 1770
Abstract
This comprehensive review explores the emerging field of epigenetics in intracranial aneurysm (IA) and aneurysmal subarachnoid hemorrhage (aSAH). Despite recent advancements, the high mortality of aSAH needs an understanding of its underlying pathophysiology, where epigenetics plays a crucial role. This review synthesizes the [...] Read more.
This comprehensive review explores the emerging field of epigenetics in intracranial aneurysm (IA) and aneurysmal subarachnoid hemorrhage (aSAH). Despite recent advancements, the high mortality of aSAH needs an understanding of its underlying pathophysiology, where epigenetics plays a crucial role. This review synthesizes the current knowledge, focusing on three primary epigenetic mechanisms: DNA methylation, non-coding RNA (ncRNA), and histone modification in IA and aSAH. While DNA methylation studies are relatively limited, they suggest a significant role in the pathogenesis and prognosis of IA and aSAH, highlighting differentially methylated positions in genes presumably involved in these pathologies. However, methodological limitations, including small sample sizes and a lack of diverse population studies, temper these results. The role of ncRNAs, particularly miRNAs, has been more extensively studied, but there are still few studies focused on histone modifications. Despite methodological challenges and inconsistent findings, these studies underscore the involvement of miRNAs in key pathophysiological processes, including vascular smooth muscle regulation and the inflammatory response. This review emphasizes methodological challenges in epigenetic research, advocating for large-scale epigenome-wide association studies integrating genetic and environmental factors, along with longitudinal studies. Such research could unravel the complex mechanisms behind IA and aSAH, guiding the development of targeted therapeutic approaches. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Acute Stroke 2.0)
Show Figures

Figure 1

Back to TopTop