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(Circulation Research. 2008;103:1202.)
© 2008 American Heart Association, Inc.

Editorials

"B₂ or not B₂?"

Kinin Receptors and Endothelial Progenitor Cell Dysfunction

Michael R. Ward, Jessie Lavoie, Duncan J. Stewart

From the St. Michael’s Hospital (M.R.W.), University of Toronto; and Ottawa Health Research Institute (J.L., D.J.S.), University of Ottawa, Ontario, Canada.

Correspondence to Duncan J. Stewart, Ottawa Health Research Institute, University of Ottawa, 725 Parkdale Avenue, Ottawa, Ontario, K1Y 4E9 Canada. E-mail stewartd@smh.toronto.on.ca

Key Words: endothelial progenitor cells • myocardial infarction • cell therapy • bradykinin • risk factors

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

The field of progenitor cell therapy appears to be poised to transform the management of many cardiovascular diseases. In particular, the use of bone marrow-derived mononuclear cells (BM-MNCs) and endothelial progenitor cells (EPCs) have shown indications of improved cardiac function post–myocardial infarction (MI), with a recent metaanalysis showing a highly significant mean improvement in global ejection fraction of 3% compared to control.¹ The overall positive results from these early trials raise 2 important questions. The first is whether cell therapy really works, in other words, whether the results of these smaller trials, which generally enrolled less than 100 patients, will be reproducible in larger pivotal studies. A study currently being planned by Zeiher and colleagues (A.M. Zeiher, personal communication) will help answer this question. The second question is whether we can do better, either by selecting a more active subset of highly regenerative progenitor cells, or by enhancing progenitor cell activity before delivery. Several clinical studies exploring these strategies are already planned or underway, including our own ENACT-AMI (eNOS and Cell Therapy Acute MI) trial. To inform further clinical studies, it is also critical to better understand progenitor cell biology, including the mechanisms by which they exert their function in vivo, as well as the genomic and proteomic interactions that underlie their survival, homing, and differentiation.

In this issue of Circulation Research, Kränkel et al² demonstrate a novel pathway that may contribute importantly to EPC function and provide a potential marker of regenerative activity. They report that the kinin . . . [Full Text of this Article]