REVIEW article
Front. Immunol.
Sec. Inflammation
This article is part of the Research TopicInflammation as a fundamental mechanism of strokeView all articles
Immune-Mediated Blood-Brain Barrier Disruption After Ischemic Stroke: Mechanisms and Therapeutic Targets
Provisionally accepted
- 1Department of Vascular and Endovascular Surgery, The First Affiliated Hospital of Yangtze University, Jingzhou, China
- 2Department of Pharmacology, School of Medicine, Yangtze University, Jingzhou, China
- 3Department of Anesthesiology, Jingzhou Hospital Affiliated to Yangtze University, Jingzhou, China
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Ischemic stroke is an acute cerebrovascular disorder characterized by the obstruction of cerebral arteries, leading to focal cerebral ischemia and infarction, ultimately resulting in neurological deficits. Its pathogenesis involves a cascade of immune-inflammatory responses and blood-brain barrier (BBB) disruption. Emerging evidence highlights that immune inflammation is a central driver of post-stroke brain injury. Microglial activation, neutrophil infiltration, and the release of pro-inflammatory cytokines collectively exacerbate BBB breakdown and neuronal death. Concurrently, these immune processes participate in tissue remodeling and repair. Notably, the interplay between immune-mediated inflammation and BBB damage forms a vicious cycle that aggravates neurological outcomes and hampers recovery. This review focuses on the molecular mechanisms of ischemia and hypoxia-induced BBB dysfunction, and the immunological processes involved, aiming to provide insights into multi-target and temporally precise neuroprotective strategies for ischemic stroke.
Keywords: ischemic stroke, Blood-Brain Barrier, immune inflammation, Neutrophil, Pro-inflammatory factor
Received: 30 Sep 2025; Accepted: 26 Nov 2025.
Copyright: © 2025 Wang, Yiqiang, Cai and Guo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Jie Cai
Jiawei Guo
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