Molecular strategies to inhibit restenosis: modulation of the vascular myocyte phenotype.
The transduction of vascular myocytes with exogenous genetic material will be a common feature of many gene-based therapies for cardiovascular disorders. Therefore, the successful application of cardiovascular gene therapy will require a thorough understanding of the molecular biology of the smooth muscle cell. Of key importance are the transcriptional regulatory events that coordinate the de-differentiation and proliferation of myocytes in response to vascular injury. The goal of this review is to highlight what is known about the regulators of vascular myocyte transcription that may serve as candidate genes for the development of genetic strategies to manage postinterventional restenosis.
Walsh
K
K
Division of Cardiovascular Research, St. Elizabeth's Medical Center, Boston, MA 02135, USA.
Perlman
H
H
D000800:Angioplasty, Balloon / Q000009:adverse effects; D000818:Animals; D003327:Coronary Disease / Q000209:etiology / Q000378:metabolism / Q000628:therapy*; D004268:DNA-Binding Proteins / Q000235:genetics; D015316:Genetic Therapy; D018398:Homeodomain Proteins / Q000235:genetics; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology; D009124:Muscle Proteins / Q000235:genetics; D009131:Muscle, Smooth, Vascular / Q000378:metabolism* / Q000503:physiopathology; D009687:Nuclear Proteins / Q000235:genetics; D010641:Phenotype; D055502:Secondary Prevention; D026362:Serum Response Factor; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics*
D004268:DNA-Binding Proteins; D018398:Homeodomain Proteins; C081336:Meox2 protein, rat; D009124:Muscle Proteins; D009687:Nuclear Proteins; D026362:Serum Response Factor; D014157:Transcription Factors