(Circulation. 1999;99:2614-2616.)
© 1999 American Heart Association, Inc.
Editorial |
From the Division of Cardiology and Sealy Center for Molecular Cardiology, University of Texas Medical Branch, Galveston, Tex.
Correspondence to Marschall S. Runge, MD, PhD, University of Texas Medical Branch, 9.138 Medical Research Bldg, 301 University Blvd, Galveston, TX 77555-1064. E-mail mrunge@utmb.edu
Key Words: : Editorials growth substances angiogenesis atherosclerosis
Approximately 15 million patients suffer from coronary and peripheral atherosclerotic diseases in the United States alone.1 The evolving development of medical and surgical therapies has significantly improved the physician's ability to manage these patients, yet many continue to suffer debilitating symptoms from their disease and remain at risk for myocardial infarction, limb loss, and death. This clinical imperative, coupled with rapid advances in molecular biology, has led to the exploration of a plethora of therapeutic angiogenesis strategies. A method described in this issue of Circulation2 offers yet another means by which angiogenesis may be achieved and thus potentially opens a new chapter in the ongoing search for novel approaches for the treatment of ischemia.
Angiogenic and Antiangiogenic Therapy
In placing the novelty of the approach by Kanno et al into
perspective, it is worth considering the important advances made during
the last decade in the field of therapeutic angiogenesis. The
investigators at the forefront of this field have not used a
traditional pharmaceutical approach to search for potential angiogenic
agents effective against vascular disease. Instead, they have chosen to
arm themselves with the fruits of the molecular biology revolution by
harnessing the power of endogenous human angiogenic
factors. Vascular endothelial growth factor (VEGF) is
the most potent and specific endogenous angiogenic factor
yet identified, so it makes sense that it would have drawn the
attention of cardiologists interested in angiogenic therapies. The
demonstration that intra-arterial injection of recombinant
VEGF could induce collateral formation in ischemic rabbit
hindlimbs3 suggested that VEGF would be a useful
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