# Mechanisms and potential therapeutic molecular targets in blood–brain barrier disruption following subarachnoid hemorrhage: a review of early brain injury

## TL;DR

This paper reviews how the blood-brain barrier breaks down after subarachnoid hemorrhage and explores new ways to treat this early brain injury.

## Contribution

The paper offers a comprehensive review of mechanisms and novel therapeutic targets for blood-brain barrier disruption following subarachnoid hemorrhage.

## Key findings

- Blood-brain barrier disruption is a key contributor to early brain injury after subarachnoid hemorrhage.
- Dysfunction of endothelial cells, tight junctions, astrocytes, and pericytes is involved in barrier breakdown.
- New molecular targets and treatments for restoring barrier integrity are being explored.

## Abstract

Subarachnoid hemorrhage (SAH) is a devastating stroke characterized by acute onset, severe symptoms, and a poor prognosis. A series of pathological changes occur within 72 h after SAH, leading to early brain injury (EBI). Blood–brain barrier (BBB) disruption is a key factor contributing to the EBI progression. When the BBB is compromised, detrimental substances and immune cells have the potential to infiltrate brain tissues, and a range of mechanisms contribute to the disruption of the BBB following SAH. This review provides a comprehensive overview of the current knowledge regarding the underlying mechanisms and potential therapeutic targets in BBB disruption during EBI following SAH. It focuses on the dysfunction of endothelial cells, tight junctions, astrocytes, and pericytes; the specific molecular targets for EBI after SAH; and new emerging treatments for BBB disruption in EBI after SAH.