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Articles in PresS, published online ahead of print October 29, 2001
Physiol Genomics, 10.1152/physiolgenomics.00073.2001
Submitted on August 27, 2001
Accepted on October 6, 2001
1 Physiology & Functional Genomics, Univ. of Florida Brain Institute, Gainesville, FL, USA
2 Surgery, Massachusetts General Hospital/Harvard Med School, Boston, MA, USA; Medicine, Brigham & Women's Hospital/Harvard Med School, Boston, MA, USA
3 Medicine, Brigham & Women's Hospital/Harvard Med School, Boston, MA, USA
4 Vascular Medicine, St. Elizabeth's Med Ctr/Tuft's Univ., Boston, MA, USA
5 Vascular Medicine, St. Elizabeth's Med Ctr/Tuft's Univ., Boston, MA, USA; Cardiology, St. Elizabeth's Med Ctr/Tuft's Univ., Boston, MA, USA
6 Cardiology, St. Elizabeth's Med Ctr/Tuft's Univ., Boston, MA, USA
7 Biochemistry & Molecular Biology, Medical Univ. of South Carolina, Charleston, SC, USA
8 Pharmacodynamics, College of Pharmacy, Gainesville, FL, USA
9 Physiology & Biophysics, Univ. of Alabama at Birmingham, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: berecek{at}uab.edu.
This article is based on an Experimental Biology symposium held in April 2001 and presents the current status of gene therapy for cardiovascular diseases in experimental studies and clinical trials. Evidence for the use of gene therapy to limit neointimal hyperplasia and confer myocardial protection was presented and it was found that augmenting local nitric oxide (NO) production using gene transfer of NO synthase or interruption of cell cycle progression through a genetic transfer of cell cycle regulatory genes limited vascular smooth muscle hyperplasia in animal models and infra-inguinal bypass patients. The results of application of vascular endothelial growth factor (VEGF) gene transfer strategies for therapeutic angiogenesis in critical limb and myocardial ischemia in pilot clinical trials was reviewed. In addition, experimental evidence was presented that genetic manipulation of peptide systems (i.e., the renin angiotensin II system and the kallikrein-kinin system) was effective in the treatment of systemic cardiovascular diseases such as hypertension, heart failure and renal failure. Although, as of yet, there are no well controlled human trials proving the clinical benefits of gene therapy for cardiovascular diseases, the data presented here in animal models and in human subjects show that genetic targeting is a promising and encouraging modality, not only for the treatment and long-term control of cardiovascular diseases, but for their prevention as well.
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