Restenosis is the main complication of coronary angioplasty. Many experimental models have been developed over the last few years, reflecting very active research work in this field. The value of experimental models may be discussed under two headings: improvement in our understanding of the mechanisms of restenosis and the development of preventing strategies. The smooth muscle cell is the main cause of restenosis, experimental models having demonstrated a triple response which has been observed clinically: proliferation, migration to the intima and synthesis of the extracellular matrix. The mechanisms controlling this response are not fully understood, the most likely candidates being desendethelialisation, platelets and other circulating components of the blood, vasopressive hormones especially the renin-angiotensin system, growth factors and finally the degree of direct trauma to the smooth muscle cells. Experimental models also allow evaluation of therapeutic strategies elaborated to reduce the frequency of restenosis in clinical practice: three strategies are identifiable: systemic treatment, local treatment and genetic therapy. At the present time, none of these approaches has been clearly shown to be effective clinically though some positive results have been observed in the animal.