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[Hyperplasia of the arterial intima due to smooth muscle cell proliferation. Current data, experimental treatments and perspectives].

Restenosis after vascular surgery using bypasses or endovascular techniques for dilatation or recanalisation remains the major Achilles' heel for these techniques. The progressive decrease of vessel lumen in an anastomose leading to graft failure or after arterial transluminal angioplasty is due to a complex process: intimal hyperplasia. This process can be compared to an hypertrophic healing into the intimal layer, reducing the lumen of the vessel. This process appears shortly after surgery or dilatation, between the 3rd and the 18th month. Mechanisms leading to this process are particularly complex, involving several cells and many regulatory processes still unclear. Smooth muscle cells are the main actor by their ability to proliferate and to secrete matrix into the media layer but stimulation and control of this process appear nevertheless complicated. The present review focuses on the pathophysiology of intimal hyperplasia, on different cells acting and on their regulation. Also, we reviewed the experimental and clinical trials evaluating approaches to the prevention of intimal hyperplasia in arteries.