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Editorials |
From the Cardiovascular Division, Kings College London BHF Centre, UK.
Correspondence to Professor Qingbo Xu, Cardiovascular Division, Kings College London, 125 Coldharbour Lane, London SE5 9NU, UK. E-mail qingbo.xu@kcl.ac.uk
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Endothelial progenitor cells (EPCs) were initially identified as bone marrow–derived circulating cells expressing endothelial-specific markers.1 These progenitors may contribute to repairing denuded endothelium of injured arteries in animal models2–4 and improving neovascularization and tissue perfusion after ischemia,5–7 highlighting the potential of these cells for therapy for cardiovascular diseases. Theoretically, the benefit of EPC therapy does not appear to be solely attributable to the ability of the cells to incorporate into the endothelium and differentiate into endothelial cells to provide physically contribution to new blood vessel formation in sites, but also as a result of the additional capacity to modulate the function of preexisting vascular cells via the paracrine effects of factors released from the cells.8–10 Thus, proper retention and survival of progenitor cells within the target tissue will be crucial for successful neovascularization improvement after therapeutic application of EPCs. However, various studies aimed to investigate the homing and the long term engraftment of cells demonstrated clearly only a low percentage (1% to 30%) of infused cells are recruited and survival in target tissue/organ in animal models as well as in clinical trials for short periods.11 Therefore, strategies to improve endogenous/exogenous progenitor cell, homing, retention, and survival in target tissues to improve the efficiency of cell therapy are essential.
See accompanying article on page 571
In this issue of Atherosclerosis, Thrombosis, and Vascular Biology, Scharner et al12 demonstrate a novel apoptosis-unrelated role of Caspase-8 for EPC-mediated neovascularization that can be applied to improve the efficiency of cell therapy. The authors
Related Article:
Arterioscler Thromb Vasc Biol 2009 29: 571-578.
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