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Published on: August 30, 2020
Inflammation in Aneurysmal Subarachnoid Hemorrhage: Cause, Consequence, or Both? Focus on Pathogen Pattern
Juhana Frösén1,2,3, Pervinder Bhogal4
1Department of Clinical Medicine, Hemorrhagic Brain Pathology Research Group, Faculty of Medicine and Health Technology, Tampere University, Finland (J.F.).
Pattern recognition receptors (PPRs) and their ligands, pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), drive inflammation in intracranial aneurysms. Targeting these pathways may prevent rupture and subsequent hemorrhage.
Area of Science:
- Neuroscience
- Immunology
- Vascular Biology
Background:
- Inflammation is critical in intracranial aneurysm (IA) development, progression, and rupture, leading to aneurysmal subarachnoid hemorrhage (aSAH).
- Pattern recognition receptors (PPRs) mediate innate immunity, responding to microbial and non-microbial danger signals.
Purpose of the Study:
- To review the role of PPRs, PAMPs, and DAMPs in IA pathogenesis and aSAH-induced neuronal injury.
- To explore potential therapeutic strategies targeting these inflammatory pathways.
Main Methods:
- Narrative review of existing literature on PPRs, PAMPs, DAMPs, and intracranial aneurysms.
- Analysis of the inflammatory mechanisms involved in IA formation, progression, and rupture.
- Discussion of therapeutic targets for IA and aSAH.
Main Results:
- PPR activation by PAMPs and DAMPs contributes to excessive inflammation, cell death, and tissue remodeling in IAs.
- These inflammatory processes are implicated in IA rupture and subsequent neuronal damage following aSAH.
Conclusions:
- PPRs, PAMPs, and DAMPs are key players in the inflammatory cascade of intracranial aneurysms.
- Targeting these innate immune mediators offers promising therapeutic avenues to prevent IA rupture and aSAH-related neurological deficits.
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