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(Circulation Research. 2005;96:705.)
© 2005 American Heart Association, Inc.

Editorials

FGF Induces Hypertrophy and Angiogenesis in Hibernating Myocardium

Stephen F. Vatner

From the Cardiovascular Research Institute, and Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey–New Jersey Medical School, Newark, NJ.

Correspondence to Stephen F. Vatner, MD, Department Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey–New Jersey Medical School, 185 South Orange Avenue, MSB G609 Newark, NJ 07103. E-mail vatnersf@umdnj.edu

See related article, pages 767–775

Key Words: hypertrophy • angiogenesis • myocardium

An extract of the first 250 words of the full text is provided, because this article has no abstract.

For several years there has been considerable interest in stimulating angiogenesis by a variety of growth factors, including the family of fibroblast growth factors (FGF). FGF-5 is a protooncogene known to stimulate cell growth and proliferation in multiple cell types, including cancer.¹ The cardiac myocyte can also produce different isoforms of FGFs, eg, it has been shown that the expression of basic FGF increases in hibernating myocardium,² which was the disease state of interest in the current study published in Circulation Research.³ The most commonly cited effect of FGF-5 in the heart is to promote angiogenesis. Several studies have shown that gene transfer of FGF-5 in the heart increases vessel formation and regional blood flow.^4–6 This effect is mediated by a production of FGF-5 by the cardiac myocytes, followed by its release in the extracellular space. In addition, FGF-5 can function as an autocrine/paracrine mechanism of cardiac cell growth and as a cytoprotective mechanism against irreversible ischemic damage.⁷

Indeed, most of the prior interest on the role of FGF has been in the field of angiogenesis, where swine models of chronic ischemia have been shown to increase blood flow, presumably through angiogenesis.^4–6,8–10 In contrast, the article by Suzuki et al,³ concluded that gene therapy with FGF improved function in their swine model of hibernating myocardium, but the mechanism of the salutary effect involved "rather than angiogenesis, stimulation of hypertrophy and re-entry of a small number of myocytes into the mitotic phase of the cell cycle... "³

These observations are . . . [Full Text of this Article]

Related Article:

Adenoviral Gene Transfer of FGF-5 to Hibernating Myocardium Improves Function and Stimulates Myocytes to Hypertrophy and Reenter the Cell Cycle

Gen Suzuki, Te-Chung Lee, James A. Fallavollita, and John M. Canty, Jr
Circ. Res. 2005 96: 767-775. [Abstract] [Full Text] [PDF]