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(Circulation Research. 2004;95:7.)
© 2004 American Heart Association, Inc.

Editorials

Plasticity of Myocytes and Capillaries

A Possible Coordinating Role for VEGF

R. Sanders Williams, Brian H. Annex

From the Division of Cardiology and Department of Medicine, Durham Veterans Affairs Medical Center; and the Duke University Medical Center, Durham, NC.

Correspondence to R. Sanders Williams, Duke University Medical Center, Dean,School of Medicine, Duke University Medical Center, Box 2927, Durham, NC 27710. E-mail willi397@mc.duke.edu

See related article, pages 58–66

Key Words: ischemia • myoglobin • mitochondria • angiogenesis • peripheral vascular disease

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

Blood vessels in muscle proliferate or regress under the control of a variety of physiological and pathological stimuli. Therapeutic angiogenesis applied to the myocardium or to skeletal muscle seeks to exploit this phenomenon to treat disorders of inadequate perfusion.¹ Early results obtained from uncontrolled human trials using angiogenic agents, for example, vascular endothelial growth factor (VEGF), were promising and led to exuberant expectations. However, of the four large placebo-controlled trials of therapeutic angiogenesis that have been published,^2–5 all but one⁵ were negative, and results from a fifth trial that used an adenovirus-expressing FGF-4 have already been released as being negative. A number of reasons have been suggested to account for negative results from human angiogenesis trials: the dose of the factor, duration of expression, mode of delivery, multiple splice variants for agents, patient selection, preselected trial end-points, patient heterogeneity, endogenous angiogenesis inhibitors, and a strong placebo effect.⁶ Thus, a potential for clinical benefit from administration of angiogenic agents cannot be excluded, and greater understanding of the biological consequences evoked by such factors may yet lead to meaningful clinical applications.

In skeletal muscles, both myocytes and capillaries undergo rapid and profound remodeling in the face of changing patterns of contractile work, environmental stresses, neurohormonal stimuli, or pathological conditions. Physical changes in myocyte size and biochemical changes in metabolic capabilities of myocytes are driven primarily by changes in expression of specific sets of genes controlled by signaling pathways that are beginning to be understood.^7–12 The structure and function of the microvasculature of . . . [Full Text of this Article]

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