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Cerebrovascular Diseases: From Pathogenesis to Treatment

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 1624

Special Issue Editors


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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
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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

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Guest Editor
Neurology Department, Stroke Unit, Hospital Universitari Arnau de Vilanova de Lleida, Universitat de Lleida, Biomedical Research Institute of Lleida, Lleida, Catalonia, Spain
Interests: cerebrovascular diseases; stroke; biomarkers; animal model; omics; ischemic tolerance; remote ischemic tolerance; cognitive impairment; PROMS

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, increased release of glutamate, excess production of free radicals, and edema and inflammation; all these events eventually contribute to cell death. In contrast, in intracerebral hemorrhage, the oppression and destruction of brain tissue by hematoma is the primary cause of brain injury, but inflammation, coagulation response, and the toxicity of the released hemoglobin play a pivotal role 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.

Recently, there has been a relevant interest in disease-modifying therapies in acute stroke, and novel approaches have been attempted to enhance recovery, reducing long-term disabilities.

This Special Issue of Current Issues in Molecular Biology will explore the current knowledge and innovative concepts regarding preclinical and clinical research into stroke mechanisms, prevention, and treatment and 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 and their potential treatment. Gene and protein expression profiles after stroke and neurogenesis, angiogenesis, and neuroplasticity are other important features in stroke and should lead to the 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
Dr. Francisco Purroy
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. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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
  • treatment

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Published Papers (2 papers)

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Research

14 pages, 3021 KiB  
Article
Transmembrane-4 L-Six Family Member-1 Is Essential for Embryonic Blood Vessel Development
by Chi-Iou Lin, Anne Merley, Hiromi Wada, Jianwei Zheng and Shou-Ching S. Jaminet
Curr. Issues Mol. Biol. 2024, 46(11), 13105-13118; https://doi.org/10.3390/cimb46110781 - 18 Nov 2024
Viewed by 290
Abstract
Transmembrane-4 L-six family member-1 (TM4SF1) is a small cell surface glycoprotein that is highly and selectively expressed on endothelial cell and mesenchymal stem cell surfaces. TM4SF1 regulates cellular functions by forming protein complexes called TMED (TM4SF1-enriched microdomains) that either recruit growth-factor activated proteins [...] Read more.
Transmembrane-4 L-six family member-1 (TM4SF1) is a small cell surface glycoprotein that is highly and selectively expressed on endothelial cell and mesenchymal stem cell surfaces. TM4SF1 regulates cellular functions by forming protein complexes called TMED (TM4SF1-enriched microdomains) that either recruit growth-factor activated proteins and internalize them via microtubules to distribute the recruited molecules intracellularly or support the formation of nanopodia for intercellular interactions extracellularly. Through a genetically manipulated mouse model for global Tm4sf1 gene knockout, we demonstrate here that TM4SF1 is essential for blood vessel development. Tm4sf1-null embryos fail to develop blood vessels and experience lethality at E9.5. Tm4SF1-heterozygous embryos are smaller in body size during early embryonic development, and almost half die in utero due to intracranial hemorrhage in the intraventricular and subarachnoid space, which becomes apparent by E17.5. Surviving Tm4SF1-heterozygotes do not display overt phenotypic differences relative to wild type littermates postnatally. Together, these studies demonstrate that TM4SF1, through its molecular facilitator and nanopodia formation roles in TMED, intimately regulates blood vessel formation during embryonic development. Full article
(This article belongs to the Special Issue Cerebrovascular Diseases: From Pathogenesis to Treatment)
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15 pages, 2393 KiB  
Article
Association of Glycoprotein IIIa PlA1/A2 Polymorphism with Risk of Stroke: Updated Meta-Analysis
by Camelia Alexandra Coadă, Mihai Lupu, Iulia Florea, Stella Di Constanzo, Sara Coluccelli and Ioan Şimon
Curr. Issues Mol. Biol. 2024, 46(6), 5364-5378; https://doi.org/10.3390/cimb46060321 - 28 May 2024
Cited by 1 | Viewed by 991
Abstract
Cardiovascular diseases are the main cause of death in the world, with ischemic heart disease (i.e., myocardial infarction) and cerebrovascular disease (i.e., stroke) taking the highest toll. Advances in diagnosis and treatment have led to a significant alleviation of ischemic complications, specifically in [...] Read more.
Cardiovascular diseases are the main cause of death in the world, with ischemic heart disease (i.e., myocardial infarction) and cerebrovascular disease (i.e., stroke) taking the highest toll. Advances in diagnosis and treatment have led to a significant alleviation of ischemic complications, specifically in the realm of pharmacotherapy and interventional devices, while pharmacogenomics has yet to be fully leveraged to improve the burden of disease. Atherothrombotic events might occur earlier or respond worse to treatment in patients with genetic variants of GP IIb/IIIa. Therefore, we aimed to quantitate the involvement of the PlA2 variant in the risk of cerebral stroke events. A systematic search and meta-analysis were performed by pooling the risks of individual studies. A total of 31 studies comprising 5985 stroke patients and 7886 controls were analyzed. A meta-analysis of four studies on hemorrhagic stroke patients showed no association with the PIA2 rs5918(C) polymorphism in both fixed-effect (OR = 0.90 95%CI [0.71; 1.14]; p = 0.398) and random-effect models (OR = 0.86 95%CI [0.62; 1.20]; p-value = 0.386). The power of this analysis was below <30%, indicating a limited ability to detect a true effect. An analysis of the 28 studies on ischemic stroke revealed a significant association with the PIA2 rs5918(C) allele in both fixed-effect (OR = 1.16 95%CI [1.06; 1.27]; p = 0.001) and random-effect models (OR = 1.20 95%CI [1.04; 1.38]; p-value = 0.012), with a power of >80%. The PIA2 allele was associated with an increased risk of ischemic stroke. No association was found with hemorrhagic stroke, most likely due to the small number of available studies, which resulted in a lack of power. Full article
(This article belongs to the Special Issue Cerebrovascular Diseases: From Pathogenesis to Treatment)
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