医学
炎症
蛛网膜下腔出血
蛛网膜下腔出血
先天免疫系统
动脉瘤
免疫系统
模式识别受体
光学(聚焦)
炎症反应
病理
病理生理学
神经科学
叙述性评论
生物信息学
程序性细胞死亡
发病机制
死因
病原相关分子模式
免疫学
作者
Juhana Frösén,Pervinder Bhogal
出处
期刊:Stroke
[Lippincott Williams & Wilkins]
日期:2026-05-27
卷期号:57 (7): 1896-1907
被引量:1
标识
DOI:10.1161/strokeaha.125.051475
摘要
Inflammation plays a key role in the formation, progression, and rupture of intracranial aneurysms, leading to aneurysmal subarachnoid hemorrhage. Pathogen PPRs (pattern recognition receptors) that are activated by pathogen-derived molecules are key mediators of the innate immune response against microbes. As PPRs are activated by molecules resembling microbes, that is, pathogen-associated molecular patterns or damage-associated molecular patterns that can be of nonmicrobial origin, exposure to pathogen-associated molecular patterns and damage-associated molecular patterns may promote an excessive inflammatory response, promoting excessive cell death and tissue remodeling. We present a narrative review describing the role of PPRs, pathogen-associated molecular patterns, and damage-associated molecular patterns in the formation, progression, and eventual rupture of intracranial aneurysms, as well as in the neuronal damage caused by aneurysmal subarachnoid hemorrhage. Furthermore, we discuss putative therapeutic approaches to prevent the death and disability caused by intracranial aneurysm rupture and subsequent aneurysmal subarachnoid hemorrhage.
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