Summary
In atherogenesis and in response to vessel injury, arterial smooth muscle cells (SMCs)
are activated from a quiescent, differentiated state into an actively proliferating
and synthetic phenotype which migrate into the intima where the cells participate
in the formation of a fibrous plaque or intimal hyperplasia. The mechanisms involved
in the control of SMC function are not clear and no preventive therapy against SMC
activation is available. Interactions between SMCs and the extracellular matrix have
been shown to influence SMC structure and function through integrin-mediated signaling
processes. The SMC basement membrane is a specific form of extracellular matrix which
seems to be crucial for the maintenance of SMC quiesence and the disruption of these
interactions is part of cellular activation after atherogenic or traumatic stimuli.
This concept of “negative growth control” may constitute a future target for the development
of new strategies in the prevention of SMC activation in atherogenesis and restenosis
formation.
Key words
Smooth muscle cells - restenosis - atherogenesis - cellular activation - basement
membrane - integrins