Rhoa Kinase Inhibition With Fasudil Versus Simvastatin in Murine Models of Cerebral Cavernous Malformations.
Cerebral Cavernous Malformations: Review of the Genetic and Protein–Protein Interactions Resulting in Disease Pathogenesis
Cerebral Cavernous Malformation, Familial
Endothelial exocytosis of angiopoietin-2 resulting from CCM3 deficiency contributes to cerebral cavernous malformation
Cerebral cavernous malformations arise from endothelial gain of MEKK3–KLF2/4 signalling
CCM-3/STRIPAK promotes seamless tube extension through endocytic recycling
The cerebral cavernous malformation 3 gene is necessary for senescence induction.
CCM proteins control endothelial β1 integrin dependent response to shear stress
Strategy for identifying repurposed drugs for the treatment of cerebral cavernous malformation.
Lack of CCM1 induces hypersprouting and impairs response to flow.
Lesions from patients with sporadic cerebral cavernous malformations harbor somatic mutations in the CCM genes: evidence for a common biochemical pathway for CCM pathogenesis
Long-term natural history of incidentally discovered cavernous malformations in a single-center cohort
Clinical course of untreated pediatric brainstem cavernous malformations: hemorrhage risk and functional recovery
Association of Cardiovascular Risk Factors with Disease Severity in Cerebral Cavernous Malformation Type 1 Subjects with the Common Hispanic Mutation
Dynamic permeability and quantitative susceptibility: related imaging biomarkers in cerebral cavernous malformations.
Long-term seizure outcomes following resection of supratentorial cavernous malformations.
Research in the News: Study uncovers potential to alleviate tissue damage during strokes or transplant
Sulindac metabolites 2015