The basis of molecular strategies for treating coronary restenosis after angioplasty.
Excessive smooth muscle cell proliferation significantly contributes to restenosis, which occurs in 25% to 50% of patients within 6 months of coronary angioplasty. Because successful treatment will probably depend on our acquiring a comprehensive knowledge of the molecular and cellular mechanisms involved, this report reviews 1) information relevant to the molecular and cellular mechanisms responsible for the smooth muscle cell(s) response to vascular injury, and 2) several molecular-based therapeutic strategies currently being explored as possible approaches to the control of restenosis, including recombinant DNA technology to target delivery of cytotoxic molecules to proliferating smooth muscle cell(s), antisense strategies to inhibit expression of gene products necessary for cell proliferation and gene therapy.
Epstein
S E
SE
Cardiology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.
Speir
E
E
Unger
E F
EF
Guzman
R J
RJ
Finkel
T
T
D016375:Antisense Elements (Genetics); D002453:Cell Cycle / Q000502:physiology; D003327:Coronary Disease / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology / Q000517:prevention & control / Q000628:therapy; D015316:Genetic Therapy; D006801:Humans; D000922:Immunotoxins / Q000627:therapeutic use; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D012008:Recurrence; D015398:Signal Transduction / Q000502:physiology
D016375:Antisense Elements (Genetics); D000922:Immunotoxins