Editorials |
From the Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University, Stanford, Calif.
Correspondence to Dr Geoffrey C. Gurtner, MD, Department of Surgery, Division of Plastic and Reconstructive Surgery, Hagey Laboratory of Regenerative Medicine, Rm GK201, 257 Campus Drive, Stanford University, Stanford, CA 94305. E-mail ggurtner@stanford.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
It is believed that this new century will be the century of regenerative medicine in which chronic diseases will be reversed by therapeutics which can repair and restore function in situ.1 One prerequisite for tissue regeneration is a readily available population of cells that are both highly renewable and highly differentiable. Commonly known as stem or precursor cells, the theoretical appeal of these cells dates back more than 100 years2 but gained traction in the latter half of the 20th century with the isolation and identification of hematopoietic stem cells,3 mesenchymal stem cells,4 and human embryonic stem cells.5,6 In vascular biology progenitor cells able to initiate neovascularization, known as endothelial precursor cells (EPCs), were first identified by Isner and Asahara7 in 1997.
See ATVB 2008;28:644–650
Since then, a number of studies have indicated a strong correlation between cardiovascular risk factors and EPC numbers and function.8 Diabetes mellitus,9,10 hypercholesterolemia,11 coronary artery disease,12 and cigarette smoking13,14 have all been shown to adversely affect EPC number and function, and it has been suggested that EPC number might be useful as a surrogate measure of vascular health.8 There has also been enthusiasm for the use of EPCs as therapeutic agents. Ex vivo isolation of EPCs and local delivery has been used to treat hindlimb ischemia,15 neointimal hyperplasia,16 and pulmonary hypertension17 in animal models. In addition, EPCs have been shown to significantly decrease left ventricular scarring and increase vascular density in animal models of myocardial infarction.18
Despite this, significant problems exist that have prevented rapid
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