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Molecular Research on Stroke

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: 20 June 2026 | Viewed by 1633

Special Issue Editor


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Guest Editor
Department of Neurology, Chungnam National University Sejong Hospital and College of Medicine, Sejong 30099, Republic of Korea
Interests: ischemic stroke; ultrasound; neuromodulation; cerebral hemodynamics

Special Issue Information

Dear Colleagues,

This Special Issue aims to highlight recent advances in molecular research on stroke, with a particular emphasis on neuroinflammation and the role of microglia. Stroke triggers a complex cascade of molecular and cellular events, including ischemic injury, oxidative stress, and immune responses. Among these, microglia—the resident immune cells of the central nervous system—play a central role in orchestrating both protective and detrimental processes depending on the spatiotemporal context. We invite original research articles and reviews that explore molecular mechanisms underlying stroke pathophysiology, including microglial activation, phenotypic transitions, cytokine signaling, and interactions with other neural and vascular components. This Special Issue aims to provide a comprehensive platform for scientists and clinicians working to understand the cellular and molecular basis of stroke and to identify novel therapeutic targets.

Prof. Dr. Hee-Jung Song
Guest Editor

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Keywords

  • stroke
  • microglia
  • neuroinflammation
  • molecular mechanisms
  • ischemic injury

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Published Papers (1 paper)

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Research

15 pages, 636 KB  
Article
The Activity of Protectin DX, 17 HDHA and Leukotriene B4 Is Correlated with Interleukin-1β (IL-1β) and Interleukin-1 Receptor Antagonist (IL-1Ra) in the Early Subacute Phase of Stroke
by Dariusz Kotlega, Arleta Drozd, Agnieszka Zembron-Lacny, Barbara Morawin, Karina Ryterska and Malgorzata Szczuko
Int. J. Mol. Sci. 2025, 26(18), 9088; https://doi.org/10.3390/ijms26189088 - 18 Sep 2025
Cited by 1 | Viewed by 1349
Abstract
Ischemic stroke is a leading cause of mortality and disability in adults. The inflammatory cascade is driven by various inflammatory molecules, such as interleukin-1β (IL-1β), and counteracted by its antagonist, interleukin-1 receptor antagonist (IL-1Ra). Eicosanoids are inflammatory derivatives of free fatty acids. Arachidonic [...] Read more.
Ischemic stroke is a leading cause of mortality and disability in adults. The inflammatory cascade is driven by various inflammatory molecules, such as interleukin-1β (IL-1β), and counteracted by its antagonist, interleukin-1 receptor antagonist (IL-1Ra). Eicosanoids are inflammatory derivatives of free fatty acids. Arachidonic acid (AA) derivatives exhibit pro-inflammatory activity, while eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) derivatives, known as specialized pro-resolving mediators, have anti-inflammatory properties. This study aimed to analyze potential associations between eicosanoids and key inflammatory molecules, including IL-1β and its antagonist IL-1Ra. In this prospective study, we investigated inflammatory molecules in 73 ischemic stroke patients. We analyzed interactions between IL-1β, IL-1Ra, and eicosanoids as follows: resolvin E1, prostaglandin E2, resolvin D1, lipoxin A4 (5S, 6R, 15R), protectin DX, maresin 1, leukotriene B4, 18RS-HEPE, 13S-HODE, 9S-HODE, 15S-HETE, 17 HDHA, 12S-HETE, 5-oxo-ETE, and 5-HETE. In 73 ischemic stroke patients, mean IL-1β was 1.31 ± 1.54 pg/mL and IL-1Ra 810.8 ± 691.0 pg/mL. Spearman correlations showed positive associations between IL-1β and protectin DX (ρ = 0.56, p < 0.001), and 17 HDHA (ρ = 0.26, p < 0.05) and 5-oxo-ETE (ρ = 0.27, p < 0.05). IL-1Ra correlated negatively with protectin DX (ρ = −0.58, p < 0.001) and 17 HDHA (ρ = −0.29, p < 0.05), and positively with leukotriene B4 (ρ = 0.34, p < 0.005). After multivariable adjustment, associations with IL-1β lost statistical significance, whereas the inverse relationships between IL-1Ra and protectin DX/17 HDHA remained significant (p < 0.005). Despite the known anti-inflammatory roles of protectin DX and 17 HDHA, and the pro-inflammatory role of leukotriene B4, their activity in the early subacute phase of ischemic stroke appears to be influenced by complex interplays, possibly mediated by IL-1β and IL-1Ra. The activity of protectin DX, 17 HDHA, and leukotriene B4 is correlated with IL-1β and IL-1Ra levels in the early subacute phase of stroke. Full article
(This article belongs to the Special Issue Molecular Research on Stroke)
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