Targeting angiogenesis and white matter repair for enhanced functional recovery after acute ischemic stroke: A focus on the roles of glial cells
Neural network connections require adequate blood flow to deliver sufficient oxygen and glucose. Acute ischemic stroke (AIS) significantly impairs neural function due to insufficient blood flow, leading to diffuse microvascular dysfunction and compromised white matter integrity, both indicators of poor prognosis. Post-stroke neural recovery hinges on promoting neovascularization around the infarct and restoring white matter integrity. Therefore, strategies to enhance angiogenesis and white matter repair are crucial for post-stroke neuro-rehabilitation. Emerging research highlights the pivotal roles of activated microglia, astrocytes, and oligodendrocyte precursor cells in facilitating neurogenesis, angiogenesis, and neural functional recovery following cerebral ischemia. In this review, we explore the mechanisms by which these neuroglial cells contribute to angiogenesis and white matter repair after AIS. We also propose potential therapeutic strategies that target the intricate interactions at the glial cell-endothelial cell interface. A deeper understanding of oligovascular signaling in ischemic conditions could unveil novel therapeutic targets for improving outcomes after AIS.
Authors
- Panpan Geng
- Yanyun Sun (ORCID: https://orcid.org/0000-0001-5092-7590)
- Weihong Du (ORCID: https://orcid.org/0000-0001-9538-952X)
- Chun Guo (ORCID: https://orcid.org/0000-0002-1540-3166)
- Xinchun Jin (ORCID: https://orcid.org/0000-0002-5351-7914)
- Wen-Cao Liu
Institutions
- Shanxi Medical University (CN)
- Capital Medical University (CN)
- Soochow University (CN)
- Second Affiliated Hospital of Soochow University (CN)
- Shanxi Provincial People’s Hospital (CN)
- Bank of England (GB)
Publication Details
- Journal
- Journal of Cerebral Blood Flow & Metabolism
- Published
- 2025-11-03
- DOI
- https://doi.org/10.1177/0271678x251389346
- Citations
- 1
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.84