Author + information
- Received July 30, 1993
- Revision received November 29, 1993
- Accepted December 1, 1993
- Published online May 1, 1994.
- Stephen E. Epstein, MD, FACC∗,
- Edith Speir, BS,
- Ellis F. Unger, MD,
- Raul J. Guzman, MD and
- Toren Finkel, MD, PhD
- ↵∗Address for correspondence: Dr. Stephen E. Epstein, Cardiology Branch, National Heart, Lung, and Blood Institute, Building 10, Room 7B15, Belhesda, Maryland 20892.
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.
- Received July 30, 1993.
- Revision received November 29, 1993.
- Accepted December 1, 1993.