Recent studies have allowed a better understanding of the biology of restenosis. Neointimal thickening--also referred to as neointimal hyperplasia--occurs in response to experimental arterial injury. This process involves different steps which include smooth muscle cell activation, proliferation, and migration, and the production of extracellular matrix. Neointimal thickening has been identified as one of the mechanisms of restenosis after balloon angioplasty in humans. The factors which control neointimal thickening include growth factors, hormonal factors, and mechanical factors. Delinquent reendothelialization has been shown to have a permissive impact on smooth muscle cell proliferation. In addition to neointimal thickening, arterial remodeling also plays a major role in restenosis. Studies performed on animals and in human subjects have established the potential for "constrictive remodeling" to reduce the vessel lumen after angioplasty. Restenosis thus appears as a multifactorial entity that may be addressed in the future by a combined mechanical and pharmacological approach.