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Cerebrovascular Diseases: From Pathogenesis to Treatment
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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 September 2025 | Viewed by 5340

Special Issue Editors

Dr. Adria Arboix

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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
Special Issues, Collections and Topics in MDPI journals
Dr. Teresa Gasull

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
Dr. Francisco Purroy

E-Mail Website
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 (7 papers)

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Research

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15 pages, 1793 KiB  
Article
Brain Tumor-Induced Changes in Routine Parameters of the Lipid Spectrum of Blood Plasma and Its Short-Chain Fatty Acids
by Larisa Obukhova, Natalia Shchelchkova, Igor Medyanik, Konstantin Yashin, Artem Grishin, Oksana Bezvuglyak and Ilkhom Abdullaev
Curr. Issues Mol. Biol. 2025, 47(4), 228; https://doi.org/10.3390/cimb47040228 - 26 Mar 2025
Viewed by 235
Abstract
The aim of this research was to provide a comparative analysis of the major parameters of the blood lipid spectrum found both in the case of brain tumors and in atherosclerosis, as well as to assess the correlation of these indicators with the [...] Read more.
The aim of this research was to provide a comparative analysis of the major parameters of the blood lipid spectrum found both in the case of brain tumors and in atherosclerosis, as well as to assess the correlation of these indicators with the proliferative activity index Ki-67 in cells. Blood analyses were conducted on samples from 50 patients with brain tumors and 50 patients with cerebral atherosclerosis. Blood plasma from 50 essentially healthy people was used for controls. Significant differences were found in the parameter values between the atherosclerosis sufferers and the control group only for their ratios of neutral lipids to cholesterol. Of the short-chain fatty acids, butyric acid is of greatest interest due to the significant differences of its levels from the control group in the blood of both patients with meningiomas and of those with gliomas. Statistically significant correlation coefficients between the levels of the Ki-67 cell proliferation marker and, in particular, butyric acid were found when compared with the neutral lipids to cholesterol ratios. These identified parameters of the blood plasma lipid spectrum can be used for preoperative diagnostics of brain tumors. However, these ratios cannot be used as preoperative noninvasive predictors of the level of the Ki-67 mitotic index, as no significant differences corresponding to this were found for low-grade or for high-grade anaplasia of brain tumors. Full article
(This article belongs to the Special Issue Cerebrovascular Diseases: From Pathogenesis to Treatment)
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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 900
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 2 | Viewed by 1357
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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Review

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28 pages, 339 KiB  
Review
The Role of HSP47 in Thrombotic Disorders: Molecular Mechanism and Therapeutic Potential
by Minodora Teodoru, Oana-Maria Stoia, Maria-Gabriela Vladoiu and Alexandra-Kristine Tonch-Cerbu
Curr. Issues Mol. Biol. 2025, 47(4), 283; https://doi.org/10.3390/cimb47040283 - 17 Apr 2025
Viewed by 152
Abstract
This review aims to analyze the role of heat shock protein 47 (HSP47) in thrombosis and evaluate its potential as a therapeutic target for deep vein thrombosis (DVT). A systematic literature review was conducted using PubMed, Scopus, and Web of Science to identify [...] Read more.
This review aims to analyze the role of heat shock protein 47 (HSP47) in thrombosis and evaluate its potential as a therapeutic target for deep vein thrombosis (DVT). A systematic literature review was conducted using PubMed, Scopus, and Web of Science to identify studies on HSP47, thrombosis, and collagen, selecting only relevant and methodologically rigorous articles. HSP47 regulates platelet function and collagen interaction, playing a key role in deep vein thrombosis (DVT). HSP47, known for stabilizing collagen, also improves platelet–collagen binding and thrombus formation. In addition, reduced HSP47 levels reduce platelet adhesion, resulting in reduced thrombus formation, while inhibitors that target HSP47 decrease platelet aggregation in animal models. Naturally low levels of HSP47 during prolonged immobility are also found in hibernating mammals, such as bears, and are associated with reduced formation of thrombi, indicating a possible natural mechanism of thrombo-protection. This observation could inform new therapeutic approaches. Current studies use in vitro platelet aggregation assays, flow chamber assays, and collagen binding studies to investigate the role of HSP47 in clotting. This review aims to synthesize existing evidence to better understand HSP47’s role in clot formation and explore its potential as a target for novel DVT therapies. Full article
(This article belongs to the Special Issue Cerebrovascular Diseases: From Pathogenesis to Treatment)
23 pages, 2104 KiB  
Review
Cerebral Small Vessel Disease: Therapeutic Approaches Targeting Neuroinflammation, Oxidative Stress, and Endothelial Dysfunction
by Habibe Yılmaz and Ulvi Bayraktutan
Curr. Issues Mol. Biol. 2025, 47(4), 232; https://doi.org/10.3390/cimb47040232 - 27 Mar 2025
Viewed by 347
Abstract
Cerebral small vessel disease (cSVD) is a common cause of stroke and dementia. Ageing, hypertension, hyperglycaemia, and smoking make up the biggest risk factors for cSVD. They individually or collectively increase the levels of reactive oxygen species, pro-inflammatory cytokines and matrix metalloproteinases, decrease [...] Read more.
Cerebral small vessel disease (cSVD) is a common cause of stroke and dementia. Ageing, hypertension, hyperglycaemia, and smoking make up the biggest risk factors for cSVD. They individually or collectively increase the levels of reactive oxygen species, pro-inflammatory cytokines and matrix metalloproteinases, decrease the bioavailability of nitric oxide, and, in the process, compromise the structural integrity and function of the vascular endothelium, blood–brain barrier, and brain parenchyma. These then appear as white matter hyperintensities, enlarged perivascular spaces, cerebral microbleeds, and atrophy in cerebral imaging. As there is currently no curative therapy for cSVD, prevention or delay of cSVD remains of particular importance to preserve quality of life for as long as possible. Bearing that in mind, this review explores whether drugs used for other neurovascular conditions may prevent neuroinflammation and oxidative damage and effectively maintain endothelial function and blood–brain barrier integrity. It also examines whether potential benefits may be extended to cSVD. The list of drugs includes anti-anginal drugs, acetylcholine esterase inhibitors, β-hydroxy β-methylglutaryl-CoA reductase inhibitors, lithium drugs, phosphodiesterase inhibitors, oral antihyperglycaemic drugs, and tetracycline antibiotics. This review discusses the mechanisms of action of these agents and critically evaluates preclinical, translational, and clinical research pertaining to cSVD. Full article
(This article belongs to the Special Issue Cerebrovascular Diseases: From Pathogenesis to Treatment)
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15 pages, 326 KiB  
Review
From Molecular to Clinical Implications of Sleep-Related Breathing Disorders on the Treatment and Recovery of Acute Stroke: A Scoping Review
by Karol Uscamaita, Olga Parra Ordaz, Imán Yazbeck Morell, Marta García Pla, María-José Sánchez-López and Adrià Arboix
Curr. Issues Mol. Biol. 2025, 47(3), 138; https://doi.org/10.3390/cimb47030138 - 21 Feb 2025
Viewed by 531
Abstract
(1) Background: The aim of this review is to map research into the molecular mechanisms linking sleep-related breathing disorders (SRBDs) and acute stroke and their clinical and therapeutic implications and to identify existing knowledge gaps to suggest new areas of research. (2) Methods: [...] Read more.
(1) Background: The aim of this review is to map research into the molecular mechanisms linking sleep-related breathing disorders (SRBDs) and acute stroke and their clinical and therapeutic implications and to identify existing knowledge gaps to suggest new areas of research. (2) Methods: This review was conducted according to the PRISMA extension for scoping reviews (PRISMA-ScR) and a predetermined protocol shared among all authors. (3) Results: The review of the thirteen studies analyzed provides a focused view of the molecular features about interaction between obstructive sleep apnea (OSA) and acute stroke. Our review identifies and highlights the biomarkers most frequently found to be associated with acute stroke, SRBDs, and their clinical repercussions. (4) Conclusions: The association between the presence of sleep apnea, especially in its severe form, and elevated levels of inflammatory markers in patients with acute stroke is highlighted and new research topics in this area are proposed. Full article
(This article belongs to the Special Issue Cerebrovascular Diseases: From Pathogenesis to Treatment)
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18 pages, 779 KiB  
Review
Neurological Sequelae of Post-COVID-19 Fatigue: A Narrative Review of Dipeptidyl Peptidase IV-Mediated Cerebrovascular Complications
by Che Mohd Nasril Che Mohd Nassir, Muhammad Danial Che Ramli, Usman Jaffer, Hafizah Abdul Hamid, Muhammad Zulfadli Mehat, Mazira Mohamad Ghazali and Ebrahim Nangarath Kottakal Cheriya
Curr. Issues Mol. Biol. 2024, 46(12), 13565-13582; https://doi.org/10.3390/cimb46120811 - 28 Nov 2024
Cited by 1 | Viewed by 1383
Abstract
Coronavirus disease 2019 (COVID-19) has been a global pandemic affecting millions of people’s lives, which has led to ‘post-COVID-19 fatigue’. Alarmingly, severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) not only infects the lungs but also influences the heart and brain. Endothelial cell dysfunction and [...] Read more.
Coronavirus disease 2019 (COVID-19) has been a global pandemic affecting millions of people’s lives, which has led to ‘post-COVID-19 fatigue’. Alarmingly, severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) not only infects the lungs but also influences the heart and brain. Endothelial cell dysfunction and hypercoagulation, which we know occur with this infection, lead to thrombo-inflammation that can manifest as many myriad cardio-cerebrovascular disorders, such as brain fog, fatigue, cognitive dysfunction, etc. Additionally, SARS-CoV-2 has been associated with oxidative stress, protein aggregation, cytokine storm, and mitochondrial dysfunction in neurodegenerative diseases. Accordingly, the identification of molecular targets involved in these actions could provide strategies for preventing and treating this disease. In particular, the very common enzyme dipeptidyl peptidase IV (DPPIV) has recently been identified as a candidate co-receptor for the cell entry of the SARS-CoV-2 virus with its involvement in infection. In addition, DPPIV has been reported as a co-receptor for some viruses such as Middle East respiratory syndrome-coronavirus (MERS-CoV). It mediates immunologic reactions and diseases such as type 2 diabetes mellitus, obesity, and hypertension, which have been considered the prime risk factors for stroke among other types of cardio-cerebrovascular diseases. Unlike angiotensin-converting enzyme 2 (ACE2), DPPIV has been implicated in aggravating the course of infection due to its disruptive effect on inflammatory signaling networks and the neuro–glia–vascular unit. Regarding the neurological, physiological, and molecular grounds governing post-COVID-19 fatigue, this review focuses on DPPIV as one of such reasons that progressively establishes cerebrovascular grievances following SARS-CoV infection. Full article
(This article belongs to the Special Issue Cerebrovascular Diseases: From Pathogenesis to Treatment)
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