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Updated: Jul 29, 2025

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
Published on: September 4, 2017
Kinases in cerebral cavernous malformations: Pathogenesis and therapeutic targets
Chunxiao Qi1, Richard Sean Bujaroski2, Jonathan Baell3
1Department of Pharmacology and Tianjin Key Laboratory of Inflammation Biology, School of Basic Medical Sciences, Tianjin Medical University, 300070, China.
Abstract:
Cerebral cavernous malformations (CCMs) are low-flow, hemorrhagic vascular lesions of the central nervous system of genetic origin, which can cause stroke-like symptoms and seizures. From the identification of CCM1, CCM2 and CCM3 as genes related to disease progression, molecular and cellular mechanisms for CCM pathogenesis have been established and the search for potential drugs to target CCM has begun. Broadly speaking, kinases are the major group signaling in CCM pathogenesis. These include the MEKK3/MEK5/ERK5 cascade, Rho/Rock signaling, CCM3/GCKIII signaling, PI3K/mTOR signaling, and others. Since the discovery of Rho/Rock in CCM pathogenesis, inhibitors for Rho signaling and subsequently other components in CCM signaling were discovered and applied in preclinical and clinical trials to ameliorate CCM progression. This review discusses the general aspects of CCM disease, kinase-mediated signaling in CCM pathogenesis and the current state of potential treatment options for CCM. It is suggested that kinase target drug development in the context of CCM might facilitate and meet the unmet requirement - a non-surgical option for CCM disease.
Insights
Cerebral cavernous malformations (CCMs) involve genetic pathways and kinase signaling. Targeting these pathways offers a promising non-surgical treatment option for CCM disease.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Cerebral cavernous malformations (CCMs) are genetic vascular lesions in the central nervous system causing stroke-like symptoms and seizures.
- Identification of CCM1, CCM2, and CCM3 genes has elucidated molecular mechanisms underlying CCM pathogenesis.
Purpose of the Study:
- To review the general aspects of CCM disease.
- To discuss kinase-mediated signaling pathways involved in CCM pathogenesis.
- To explore current potential therapeutic strategies for CCM.
Main Methods:
- Literature review of CCM disease mechanisms and signaling pathways.
- Analysis of kinase signaling cascades (e.g., MEKK3/MEK5/ERK5, Rho/Rock, CCM3/GCKIII, PI3K/mTOR).
- Examination of preclinical and clinical trial data for CCM therapeutics.
Main Results:
- Kinases play a central role in CCM pathogenesis, with several key signaling cascades identified.
- Inhibitors targeting Rho/Rock signaling and other kinase components have shown potential in preclinical and clinical studies.
- Drug development targeting kinase signaling pathways is advancing.
Conclusions:
- Kinase-targeted drug development presents a viable non-surgical treatment option for CCM disease.
- Further research into kinase inhibitors may address the unmet need for effective CCM therapies.
- Understanding kinase signaling is crucial for developing novel therapeutic interventions for CCM.
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