Advances in the Study of KRAS in Brain Arteriovenous Malformation

• Published in: Cerebrovascular diseases (Basel, Switzerland) Vol. 53; no. 6; p. 767
• Main Authors: Pang, Miao, Zhang, Guanghao, Shang, Chenghao, Zhang, Yuhang, Chen, Rundong, Li, Zhe, Ding, Xin, Duan, Guoli, Li, Qiang
• Format: Journal Article
• Language: English
• Published: Switzerland 01.01.2025
• Subjects: Angiogenesis Inhibitors - therapeutic use; Animals; Endothelial Cells - metabolism; Endothelial Cells - pathology; Genetic Predisposition to Disease; Humans; Intracranial Arteriovenous Malformations - genetics; Intracranial Arteriovenous Malformations - metabolism; Mutation; Neovascularization, Pathologic - genetics; Phenotype; Proto-Oncogene Proteins p21(ras) - genetics; Signal Transduction; Angiogenesis; Endothelial cell; KRAS; Brain arteriovenous malformation; Somatic mutations; Therapeutic targets
• ISSN: 1421-9786
• DOI: 10.1159/000535139

Brain arteriovenous malformation (bAVM) is an abnormal vascular mass with disordered arteriovenous connection. Endothelial KRAS mutation is common in bAVM. In vivo studies have demonstrated that mutations of KRAS in somatic cells can induce bAVM-like angiogenesis, suggesting that KRAS gene may play a key role in the development and progression of bAVM. In this article, we will provide a comprehensive review of action mechanisms of KRAS mutations in the development of bAVM and summarize potential targeting drugs for KRAS mutations in bAVM somatic cells. KRAS mutation in human brain endothelial cells is a key driver in the pathogenesis of sporadic cerebral arteriovenous malformations. It is of great clinical importance to explore and summarize the changes in the signaling pathway induced by KRAS mutation, which may provide additional targets for the treatment of sporadic bAVM development.