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Molecular Pathogenesis of Ischemic and Hemorrhagic Strokes

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 August 2024) | Viewed by 2608

Special Issue Editor

Special Issue Information

Dear Colleagues,

Based on its etiology, stroke can be classified into ischemic or hemorrhagic subtypes. Hypertension, diabetes, obesity, dyslipidemia, physical inactivity and cardiovascular disorders are the main modifiable risk factors.

Understanding the molecular mechanisms mediating each of these risk factors is expected to contribute significantly to reducing stroke risk, preventing neural damage, improving rehabilitation, and designing appropriate treatments. Abnormalities in the structure of the blood–brain barrier and blood vessels, thrombosis, vasoconstriction, atherosclerosis, reduced cerebral blood flow, neural oxidative stress, inflammation and apoptosis, reduced synaptic transmission, excitotoxicity, and altered expression/activity of many signaling channels and proteins are the best known mechanisms responsible for stroke induction.

The role of cerebral amyloid angiopathy (CAA) in hemorrhagic stroke has not yet been fully elucidated, and its role in ischemic stroke also remains unclear and worthy of further investigation.

This Special Issue of the International Journal of Molecular Sciences entitled “Molecular Pathogenesis of Ischemic and Hemorrhagic Strokes” will present studies that address the molecular pathogenesis of cerebrovascular damage due to the principal cerebrovascular risk factors such as hypertension, diabetes, dyslipidemia, inflammation, and physical inactivity. This Special Issue will also showcase research that focuses on the role of amyloid angiopathy in the pathogenesis of hemorrhagic stroke and examines the possible role of amyloid as possible pathogenetic stroke in vascular damage mechanisms linked to the different subtypes of ischemic stroke.

Prof. Dr. Antonino Tuttolomondo
Guest Editor

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Keywords

  • stroke
  • ischemic stroke
  • hemorrhagic stroke
  • hypertension
  • dyslipidemia
  • cerebral amyloid angiopathy

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Published Papers (1 paper)

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Review

40 pages, 2577 KiB  
Review
Molecular Pathways of Vulnerable Carotid Plaques at Risk of Ischemic Stroke: A Narrative Review
by Giuseppe Miceli, Maria Grazia Basso, Chiara Pintus, Andrea Roberta Pennacchio, Elena Cocciola, Mariagiovanna Cuffaro, Martina Profita, Giuliana Rizzo and Antonino Tuttolomondo
Int. J. Mol. Sci. 2024, 25(8), 4351; https://doi.org/10.3390/ijms25084351 - 15 Apr 2024
Cited by 5 | Viewed by 2015
Abstract
The concept of vulnerable carotid plaques is pivotal in understanding the pathophysiology of ischemic stroke secondary to large-artery atherosclerosis. In macroscopic evaluation, vulnerable plaques are characterized by one or more of the following features: microcalcification; neovascularization; lipid-rich necrotic cores (LRNCs); intraplaque hemorrhage (IPH); [...] Read more.
The concept of vulnerable carotid plaques is pivotal in understanding the pathophysiology of ischemic stroke secondary to large-artery atherosclerosis. In macroscopic evaluation, vulnerable plaques are characterized by one or more of the following features: microcalcification; neovascularization; lipid-rich necrotic cores (LRNCs); intraplaque hemorrhage (IPH); thin fibrous caps; plaque surface ulceration; huge dimensions, suggesting stenosis; and plaque rupture. Recognizing these macroscopic characteristics is crucial for estimating the risk of cerebrovascular events, also in the case of non-significant (less than 50%) stenosis. Inflammatory biomarkers, such as cytokines and adhesion molecules, lipid-related markers like oxidized low-density lipoprotein (LDL), and proteolytic enzymes capable of degrading extracellular matrix components are among the key molecules that are scrutinized for their associative roles in plaque instability. Through their quantification and evaluation, these biomarkers reveal intricate molecular cross-talk governing plaque inflammation, rupture potential, and thrombogenicity. The current evidence demonstrates that plaque vulnerability phenotypes are multiple and heterogeneous and are associated with many highly complex molecular pathways that determine the activation of an immune-mediated cascade that culminates in thromboinflammation. This narrative review provides a comprehensive analysis of the current knowledge on molecular biomarkers expressed by symptomatic carotid plaques. It explores the association of these biomarkers with the structural and compositional attributes that characterize vulnerable plaques. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Ischemic and Hemorrhagic Strokes)
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