Vascular smooth muscle cells (VSMCs) are the predominant cell type within blood vessels. In normal vessels VSMC have low rates of proliferation, migration and apoptosis. However, increased VSMC proliferation, migration, and apoptosis rates radically alter the composition and structure of the blood vessel wall and contribute to vascular diseases such as atherosclerosis, in-stent restenosis and vein graft failure. Consequently, therapies that modulate VSMC proliferation, migration and apoptosis may be useful for treating vascular diseases. In this review article we discuss recently emerging research that has revealed that homophilic cell-cell contacts mediated by the cadherin: catenin complex and Wnt/beta-catenin signalling are important regulators of VSMC behaviour.
- E-DEFICIENT MICE
- PROTEIN INTERACTIONS
- Vascular Smooth Muscle Cell
- ATHEROSCLEROTIC PLAQUE INSTABILITY
- GROWTH-FACTOR RECEPTOR