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A Murine Model of Carotid Aneurysm Formation
Published on: September 9, 2025
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Molecular basis for intracranial aneurysm formation.
1Department of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Acta Neurochirurgica. Supplement
|November 5, 2014
Summary
Intracranial aneurysms (IAs) are inflammatory diseases. A positive feedback loop involving COX-2, PGE2, EP2, and NF-κB signaling, triggered by hemodynamic stress and macrophage infiltration, drives IA formation.
Area of Science:
- Neuroscience
- Cardiovascular Biology
- Immunology
Background:
- Intracranial aneurysms (IAs) are a significant health concern due to high prevalence and risk of subarachnoid hemorrhage.
- Current treatments for IAs are often invasive, highlighting a need for less invasive medical therapies.
- Understanding the molecular mechanisms of IA formation is crucial for developing new treatments.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying intracranial aneurysm (IA) formation.
- To investigate the interplay between hemodynamic stress, inflammation, and IA pathogenesis.
- To propose a novel signaling pathway regulating IA development.
Main Methods:
- Utilized animal models of IA to study molecular mechanisms.
- Investigated the role of hemodynamic stress and inflammatory responses in IA pathogenesis.
- Analyzed the cyclooxygenase (COX)-2 - prostaglandin (PG) E2 - prostaglandin E receptor 2 (EP2) - nuclear factor (NF)-κB signaling pathway.
Main Results:
- Identified a positive feedback loop in IA pathogenesis.
- Demonstrated that hemodynamic stress triggers inflammation via the COX-2/PGE2/EP2/NF-κB pathway.
- Showcased NF-κB-mediated monocyte chemoattractant protein (MCP)-1 induction linked to macrophage infiltration.
Conclusions:
- Intracranial aneurysm (IA) is proposed as a chronic inflammatory disease.
- The identified signaling pathway provides a potential therapeutic target for IA treatment.
- Findings suggest future directions for developing less invasive medical therapies for IAs.
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