Faculty, Staff and Student Publications
Publication Date
8-7-2024
Journal
Biomedicines
Abstract
Brain arteriovenous malformations (bAVMs) substantially increase the risk for intracerebral hemorrhage (ICH), which is associated with significant morbidity and mortality. However, the treatment options for bAVMs are severely limited, primarily relying on invasive methods that carry their own risks for intraoperative hemorrhage or even death. Currently, there are no pharmaceutical agents shown to treat this condition, primarily due to a poor understanding of bAVM pathophysiology. For the last decade, bAVM research has made significant advances, including the identification of novel genetic mutations and relevant signaling in bAVM development. However, bAVM pathophysiology is still largely unclear. Further investigation is required to understand the detailed cellular and molecular mechanisms involved, which will enable the development of safer and more effective treatment options. Endothelial cells (ECs), the cells that line the vascular lumen, are integral to the pathogenesis of bAVMs. Understanding the fundamental role of ECs in pathological conditions is crucial to unraveling bAVM pathophysiology. This review focuses on the current knowledge of bAVM-relevant signaling pathways and dysfunctions in ECs, particularly the endothelial-to-mesenchymal transition (EndMT).
Keywords
arteriovenous malformations (AVMs), endothelial cells (ECs), endothelial dysfunction, endothelial-to-mesenchymal transition (EndMT)
DOI
10.3390/biomedicines12081795
PMID
39200259
PMCID
PMC11351371
PubMedCentral® Posted Date
8-7-2024
PubMedCentral® Full Text Version
Post-print
Published Open-Access
yes