[Treatment of intimal hyperplasia by gene therapy: an update]

Injury to the vessel wall leads to smooth muscle cell (SMC) activation followed by intimal hyperplasia (IH). This process contributes to restenosis following balloon angioplasty--particularly with stenting--occlusion of vascular bypasses, and transplant arteriopathy. Genetic interventions affecting the cell cycle or early postinjury events have been successful in limiting SMC proliferation in vitro and in animal models. Gene therapy strategies have included the use of antisense oligonucleotides that block protein synthesis, transduced "suicide" genes that cause cytotoxicity, and cells engineered genetically to reduce the response to injury. The clinical application of gene therapy in vascular diseases should become a reality with the development of new delivery systems permitting efficient gene transfer to the injured vascular wall (J Mal Vasc 1999; 24: 349-355).