Remodeling of blood-brain barrier function: implications for stroke therapy and clinical translation

Intracerebral hemorrhage (ICH), typically caused by hypertension or aneurysm rupture, is a devastating subtype of stroke. ICH accounts for approximately 15% of all stroke cases and is characterized by high mortality and morbidity. Despite advances in neurocritical care, clinical interventions such as hematoma evacuation rarely improve neurological outcomes. Studies have found that ICH causes not only primary brain injury but also secondary brain injury after hemorrhage, in which disruption of the blood-brain barrier (BBB) is a central event, contributing to peri-hematomal edema, hematoma expansion, and ultimately neuronal damage. The neurovascular unit (NVU) is the core component of the BBB and is composed of endothelial cells, astrocytes, pericytes, neurons, and the extracellular matrix.

Given the central role of BBB disruption in ICH pathophysiology, strategies aimed at limiting BBB dysfunction represent promising therapeutic targets. Understanding how the BBB can be protected or restored after hemorrhage is critical to improving patient outcomes and advancing clinical translation. Yet despite growing interest in this area, the mechanisms governing BBB remodeling remain incompletely understood, and effective BBB-targeted therapies have yet to reach the clinic. This Research Topic aims to consolidate current knowledge and stimulate new research on the remodeling of blood-brain barrier function and its implications for stroke therapy and clinical translation. A particular emphasis is placed on findings with the potential to inform therapeutic development and improve clinical outcomes for ICH patients.

We welcome original research articles, reviews, and perspectives addressing the mechanisms that govern BBB remodeling as a therapeutic strategy for ICH treatment. Contributions from both basic science and translational perspectives are encouraged, and we particularly invite work that bridges experimental findings with clinical relevance. Topics of interest include:

-Underlying mechanisms of BBB dysfunction after ICH, including oxidative stress, inflammatory response, and autophagy, as potential targets for therapeutic intervention
- The immune response in BBB remodeling after ICH
- The role of mitochondria during BBB remodeling for ICH therapy
- Potential roles and translational studies of stem cells or medications for BBB remodeling
- Novel preclinical tools and techniques for modeling and remodeling BBB function, such as organoids and organ-on-a-chip platforms