動脈硬化症における平滑筋細胞の分化機能調節 : 細胞外マトリックスの役割(<特集>動脈硬化と細胞外マトリックス)

概要

論文の詳細を見る
In the early stages of atherosclerosis, vascular smooth muscle cells (SMCs) undergo transition from the contractile to the synthetic phenotype, characterized by losing their contractility and instead regaining the capacity to proliferate and generate extracellular matrix (ECM) components. This phenotypic transition appears to be an early key event in the pathogenesis of atherosclerosis and restenosis. ECM may control vascular responses in migration, growth, and differentiation and play an important role in determining the phenotypic transition of vascular SMCs. Fibronectin and types I, III, and V collagen promote the transition to the synthetic phenotype, while laminin, type IV collagen, elastin, heparin, and heparan sulfate act in the opposite direction in phenotypic transition. The differentiated properties of the SMCs are controlled by their adherence to these ECM components through specific cell surface receptors (integrin or non-integrins). Further investigations in this field will aid in identifying the mechanisms of the pathogenesis of atherosclerosis.
2002-12-25