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Special Issue "Molecular Mechanisms of Cerebrovascular Diseases"

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: 30 June 2021.

Special Issue Editors

Prof. Dr. Anuska V. Andjelkovic
E-Mail Website
Guest Editor
1. Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA
2. Department of Neurosurgery, University of Michigan Medical School, Ann Arbor, MI, USA
Interests: blood brain barrier; stroke; neuroinflammation; vascular malformation; aging; neurodegeneration; cell junctionas; epigenetics
Prof. Dr. Richard F. Keep
E-Mail Website
Guest Editor
Department of Neurosurgery, University of Michigan, Ann Arbor, Ann Arbor, United States
Interests: hemorragic stroke; ischemic stroke; blood brain barrier; Blod-CSF barrier neuroinflamamation
Prof. Dr. Michael M. Wang
E-Mail Website
Guest Editor
University of Michigan, Ann Arbor, Ann Arbor, United States
Interests: CADASIL; vascular dementia; stroke; neuroprotectionnuclear hormone receptor molecular biology

Special Issue Information

Dear colleagues,

Cerebrovascular diseases are a heterogenous group of disorders that affect brain vasculature structure and cerebral blood flow regulation. The common pathological event related to cerebrovascular diseases is stroke, manifested as a sudden cessation of blood flow due to vessel occlusion (ischemic stroke), transient occlusion with recovery (transient ischemic attack), or vessel rupture (hemorrhagic stroke). Brain endothelial cell dysfunction, vessel wall deterioration, and perivascular environment remodeling are major pathological substrates in cerebrovascular diseases. A wide variety of conditions, risk factors, and disorders lead to cerebrovascular diseases, although the underlying molecular mechanisms remain enigmatic. This Special Issue, entitled “Molecular Mechanisms of Cerebrovascular Diseases”, is focused on the molecular mechanisms of endothelial dysfunction and perivascular environment remodeling that lead to lodging of thromboemboli, vessel occlusion and rupture, the mechanism of aging and metabolic vascular wall degeneration, vascular injury and remodeling in sporadic and inherited vascular malformations, and mechanisms of impaired cerebral autoregulation. In addition to “traditional” mechanisms (e.g., inflammation, oxidative stress), this Special Issue welcomes articles that provide an overview of the role of epigenetics, mechanotransduction, and mitochondrial molecular mechanisms in the pathogenesis of cerebrovascular diseases. Studies on the molecular mechanisms associated with cerebral small vessel disease, both sporadic and inherited (i.e., CADASIL and CARASIL), as well as rare disorders, such as MoyaMoya, venous angioma, and Vein of Galen malformation, are also welcome. As such, this Special Issue welcomes submissions of original research and review articles related to any aspect of the molecular mechanisms and pathogenesis of cerebrovascular diseases, identification and exploration of novel targets, and biomarkers.

Prof. Dr. Anuska V. Andjelkovic
Prof. Dr. Richard F. Keep
Prof. Dr. Michael M. Wang
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 papers will be 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
  • cerebrovascular malformation
  • small vessel diseases
  • inflammation
  • mitochondria
  • epigenetics
  • biomarkers

Published Papers (2 papers)

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Research

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Open AccessArticle
Hydrocephalus Following Experimental Subarachnoid Hemorrhage in Rats with Different Aerobic Capacity
Int. J. Mol. Sci. 2021, 22(9), 4489; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094489 - 26 Apr 2021
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Abstract
Low aerobic capacity is considered to be a risk factor for stroke, while the mechanisms underlying the phenomenon are still unclear. The current study looked into the impacts of different aerobic capacities on early brain injury in a subarachnoid hemorrhage (SAH) model using [...] Read more.
Low aerobic capacity is considered to be a risk factor for stroke, while the mechanisms underlying the phenomenon are still unclear. The current study looked into the impacts of different aerobic capacities on early brain injury in a subarachnoid hemorrhage (SAH) model using rats bred for high and low aerobic capacity (high-capacity runners, HCR; low-capacity runners, LCR). SAH was modeled with endovascular perforation in HCR and LCR rats. Twenty-four hours after SAH, the rats underwent behavioral testing and MRI, and were then euthanized. The brains were used to investigate ventricular wall damage, blood–brain barrier breakdown, oxidative stress, and hemoglobin scavenging. The LCR rats had worse SAH grades (p < 0.01), ventricular dilatation (p < 0.01), ventricular wall damage (p < 0.01), and behavioral scores (p < 0.01). The periventricular expression of HO-1 and CD163 was significantly increased in LCR rats (p < 0.01 each). CD163-positive cells were co-localized with HO-1-positive cells. The LCR rats had greater early brain injuries than HCR rats. The LCR rats had more serious SAH and extensive ventricular wall damage that evolved more frequently into hydrocephalus. This may reflect changes in iron handling and neuroinflammation. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cerebrovascular Diseases)
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Review

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Open AccessReview
Could Lipoxins Represent a New Standard in Ischemic Stroke Treatment?
Int. J. Mol. Sci. 2021, 22(8), 4207; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084207 - 19 Apr 2021
Viewed by 325
Abstract
Introduction: Cardiovascular diseases including stroke are one of the most common causes of death. Their main cause is atherosclerosis and chronic inflammation in the body. An ischemic stroke may occur as a result of the rupture of unstable atherosclerotic plaque. Cardiovascular diseases are [...] Read more.
Introduction: Cardiovascular diseases including stroke are one of the most common causes of death. Their main cause is atherosclerosis and chronic inflammation in the body. An ischemic stroke may occur as a result of the rupture of unstable atherosclerotic plaque. Cardiovascular diseases are associated with uncontrolled inflammation. The inflammatory reaction produces chemical mediators that stimulate the resolution of inflammation. One of these mediators is lipoxins—pro-resolving mediators that are derived from the omega-6 fatty acid family, promoting inflammation relief and supporting tissue regeneration. Aim: The aim of the study was to review the available literature on the therapeutic potential of lipoxins in the context of ischemic stroke. Material and Methods: Articles published up to 31 January 2021 were included in the review. The literature was searched on the basis of PubMed and Embase in terms of the entries: ‘stroke and lipoxin’ and ‘stroke and atherosclerosis’, resulting in over 110 articles in total. Studies that were not in full-text English, letters to the editor, and conference abstracts were excluded. Results: In animal studies, the injection/administration of lipoxin A4 improved the integrity of the blood–brain barrier (BBB), decreased the volume of damage caused by ischemic stroke, and decreased brain edema. In addition, lipoxin A4 inhibited the infiltration of neutrophils and the production of cytokines and pro-inflammatory chemokines, such as interleukin (Il-1β, Il-6, Il-8) and tumor necrosis factor-α (TNF-α). The beneficial effects were also observed after introducing the administration of lipoxin A4 analog—BML-111. BML-111 significantly reduces the size of a stroke and protects the cerebral cortex, possibly by reducing the permeability of the blood–brain barrier. Moreover, more potent than lipoxin A4, it has an anti-inflammatory effect by inhibiting the production of pro-inflammatory cytokines and increasing the amount of anti-inflammatory cytokines. Conclusions: Lipoxins and their analogues may find application in reducing damage caused by stroke and improving the prognosis of patients after ischemic stroke. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cerebrovascular Diseases)
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