Levinson Simon, Pulli Benjamin, Heit Jeremy J
Department of Neurosurgery, School of Medicine, Stanford University, Stanford, CA, United States.
Department of Radiology, School of Medicine, Stanford University, Stanford, CA, United States.
Front Surg. 2025 Apr 28;12:1501359. doi: 10.3389/fsurg.2025.1501359. eCollection 2025.
Stroke, encompassing both ischemic and hemorrhagic subtypes, is a leading cause of mortality and disability globally and current treatments remain limited. Neuroinflammation plays a crucial role in the pathophysiology of stroke, influencing both acute injury and long-term recovery.
This review aims to provide a comprehensive overview of neuroinflammation in stroke, detailing the mechanisms, clinical implications, and potential therapeutic strategies.
A detailed literature review was conducted, focusing on recent advancements in understanding the neuroinflammatory processes in stroke, including the roles of thromboinflammation, blood-brain barrier (BBB) disruption, and the immune response.
The initial ischemic insult triggers an inflammatory cascade involving both innate and adaptive immune responses. BBB disruption allows peripheral immune cells and neurotoxic substances to infiltrate the brain, exacerbating neuronal damage and increasing the risk of infections such as pneumonia and urinary tract infections. Thromboinflammation, characterized by platelet activation and immune cell interactions, further complicates the ischemic environment. Proteomic studies have identified key biomarkers that offer insights into neuroinflammatory mechanisms and potential therapeutic targets. Advances in imaging techniques, such as PET and MRI, enable real-time monitoring of neuroinflammation, facilitating personalized treatment approaches.
Neuroinflammation significantly impacts stroke outcomes, presenting both challenges and opportunities for treatment. Current immunologic therapeutic strategies are limited. Future research should aim to further elucidate the complex immune interactions in stroke, refine imaging biomarkers for clinical use, and develop effective interventions to mitigate neuroinflammation.
中风，包括缺血性和出血性亚型，是全球范围内导致死亡和残疾的主要原因，目前的治疗方法仍然有限。神经炎症在中风的病理生理学中起着至关重要的作用，影响急性损伤和长期恢复。
本综述旨在全面概述中风中的神经炎症，详细阐述其机制、临床意义和潜在的治疗策略。
进行了详细的文献综述，重点关注中风神经炎症过程理解方面的最新进展，包括血栓炎症、血脑屏障（BBB）破坏和免疫反应的作用。
最初的缺血性损伤引发了涉及固有免疫和适应性免疫反应的炎症级联反应。血脑屏障破坏使外周免疫细胞和神经毒性物质渗入大脑，加剧神经元损伤，并增加肺炎和尿路感染等感染的风险。以血小板活化和免疫细胞相互作用为特征的血栓炎症使缺血环境更加复杂。蛋白质组学研究已经确定了关键生物标志物，这些标志物为神经炎症机制和潜在治疗靶点提供了见解。正电子发射断层扫描（PET）和磁共振成像（MRI）等成像技术的进步能够实时监测神经炎症，促进个性化治疗方法的发展。
神经炎症对中风预后有显著影响，为治疗带来了挑战和机遇。目前的免疫治疗策略有限。未来的研究应旨在进一步阐明中风中复杂的免疫相互作用，完善用于临床的成像生物标志物，并开发有效的干预措施来减轻神经炎症。
