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Stroke: Novel Molecular Mechanisms and Therapeutic Approaches

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 December 2025 | Viewed by 1975

Special Issue Editor


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Guest Editor
Department of Neurology, Chonnam National University School of Medicine and Hospital, Gwangju 61469, Republic of Korea
Interests: stroke; neurodegenerative disease; headache; sleep disorder

Special Issue Information

Dear Colleagues,

The special issue "Stroke: Novel Molecular Mechanisms and Therapeutic Approaches" is a collection dedicated to exploring recent advances in the emerging molecular basis and treatment of stroke and neurotrauma.

Our focus concerns the latest updates on the pathophysiology, diagnosis, monitoring, and treatments for cerebrovascular disease. Researchers and clinicians will share their experiences and results in the latest research advances and novel therapeutic approaches. This Special Issue aims to provide the scientific community with an in-depth understanding of the pathogenesis and molecular pathways of cerebrovascular diseases to provide the basis for developing new treatments. The Special Issue will include treatment innovations in cerebrovascular disease and neurotrauma, including drug therapy, nano therapy, gene therapy, stem cell therapy, and the latest technology.

This Special Issue will comprehensively select recent research topics and review articles. We invite submissions on various issues related to novel and emerging molecular mechanisms and therapeutic approaches in stroke. These include exploratory or fundamental scientific studies, preclinical, cross-sectional, and clinical studies, and systematic and narrative/comprehensive reviews. We hope this collection will be a valuable guide for researchers and clinicians.

Dr. Kang-Ho Choi
Guest Editor

Manuscript Submission Information

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Keywords

  • stroke
  • cerebrovascular disease
  • mechanisms
  • treatment
  • diagnosis

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Published Papers (2 papers)

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Research

24 pages, 7363 KB  
Article
Preclinical Evaluation of Atorvastatin-Loaded PEGylated Liposomes in a Mouse Model of Traumatic Brain Injury
by Eun-Sol Hwang, Ja-Hae Kim, Ji-Hye Kim, Raveena Nagareddy, Yong-Yeon Jeong and Kang-Ho Choi
Int. J. Mol. Sci. 2025, 26(24), 12176; https://doi.org/10.3390/ijms262412176 - 18 Dec 2025
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Abstract
Evidence on the therapeutic use of nanoparticles for traumatic brain injury (TBI) remains limited. This study aimed to evaluate the neuroprotective potential of atorvastatin-loaded polyethylene glycol (PEG)-conjugated liposomes (LipoStatin) in a mouse model of repetitive TBI. TBI was induced using five controlled head [...] Read more.
Evidence on the therapeutic use of nanoparticles for traumatic brain injury (TBI) remains limited. This study aimed to evaluate the neuroprotective potential of atorvastatin-loaded polyethylene glycol (PEG)-conjugated liposomes (LipoStatin) in a mouse model of repetitive TBI. TBI was induced using five controlled head impacts with a 120 g weight at 12-h intervals. Mice were randomly assigned to Sham, Control (saline-treated), Statin (free atorvastatin), Liposome (empty PEGylated liposomes without atorvastatin), and LipoStatin (atorvastatin-loaded PEGylated liposome) groups. LipoStatin (10 mg/kg/day) was intravenously administered for 5 days post-injury. Neurological function was evaluated using the neurological severity score (NSS), while blood–brain barrier (BBB) integrity and neuroinflammation were assessed on day 5, and cellular apoptosis on day 12. LipoStatin-treated mice exhibited the lowest NSSs. IVIS® imaging indicated significantly attenuated BBB disruption (p < 0.001), and Western blot analysis revealed restored caveolin-1 protein levels (p < 0.01), which are associated with BBB integrity. TNF-α levels were reduced considerably in the LipoStatin group compared to both the Control (p < 0.001) and Statin (p < 0.05) groups. Immunofluorescence showed reduced co-localization of caspase-3 with PDGFR-β and GFAP, indicating decreased pericyte and astrocyte apoptosis. These findings suggest that LipoStatin may confer neuroprotection in TBI by stabilizing BBB integrity, reducing inflammation, and mitigating cell death, supporting its potential as an improved nanocarrier-based therapeutic approach. Full article
(This article belongs to the Special Issue Stroke: Novel Molecular Mechanisms and Therapeutic Approaches)
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17 pages, 5312 KB  
Article
Positive Behavioral, Morphophysiological, and Gene Expression Effects of the Administration of Virgin Coconut Oil in an Ischemic Stroke Surgical Rat Model
by Rodel Jonathan S. Vitor II, Ryota Tochinai, Shin-Ichi Sekizawa and Masayoshi Kuwahara
Int. J. Mol. Sci. 2025, 26(13), 6215; https://doi.org/10.3390/ijms26136215 - 27 Jun 2025
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Abstract
Stroke is still considered a predominant cause of morbidity and mortality, for which research on prevention and cure has been sought to prevent neuronal damage after a stroke incident. In this research, we evaluated the protective effects of virgin coconut oil (VCO) using [...] Read more.
Stroke is still considered a predominant cause of morbidity and mortality, for which research on prevention and cure has been sought to prevent neuronal damage after a stroke incident. In this research, we evaluated the protective effects of virgin coconut oil (VCO) using behavioral, morphophysiological, and gene expression parameters using an ischemic stroke surgical rat model using Sprague Dawley (SD) rats. Eight-week-old SD rats were subjected to repeated oral administration (5 mL/kg/day) of either 1% Tween 80 or VCO. For behavioral and morphophysiological parameters, surgery was performed for each group, after which neurological scoring was performed at 4 h, 24 h, 48 h, 5 d, and 10 d. Further, hematological and brain morphology assessment was performed after euthanasia and necropsy of the animals. For gene expression studies, surgery was performed with animals sacrificed at different time points (baseline, before surgery, 4 h, 24 h, and 48 h after surgery) to collect the brain. Results of the study showed that there are differences in the neurological scores between the two treatments 24 h, 48 h, and 5 d after surgery. Brain morphology assessment also showed favorable results for VCO for infarct size, edema, and hypoxic neurons. Gene expression studies also showed positive results with an increase in the relative expression of angiogenin (Ang), angiopoietin (Angpt 1), Parkin, dynamin-related protein 1 (Drp 1), mitofusin 2 (Mfn 2), and mitochondrial rho (Miro) and decreased relative expression of caspase 3, receptor for advanced glycation end-product (Rage), and glyceraldehyde-3-phosphate dehydrogenase (Gapdh). In summary, the current study shows that VCO may have protective effects on the brain after stroke, which may be explained by the results of the gene expression studies. Full article
(This article belongs to the Special Issue Stroke: Novel Molecular Mechanisms and Therapeutic Approaches)
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