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J.W. Goethe University, Frankfurt, Germany
Address correspondence to: Dr. Volker Schächinger, Medizinische Klinik IV/Kardiologie, J.W. Goethe Universität, Frankfurt Theodor-Stern-Kai 7, 60590 Frankfurt, Germany. Phone: 0049-69-6301-7387; Fax: 0049-69-6301-6546; E-mail: schaechinger{at}em.uni-frankfurt.de
The traditional view that organs have only limited regenerative capacity has been challenged in recent years as adult bone marrow stem cells as well circulating progenitor cells have been identified to retain the plasticity to participate in neovascularization, a process so far believed not to be possible after birth. An organ that is damaged by ischemia causes the release of cytokines; these act via the flowing blood and stimulate the bone marrow, which then mobilizes progenitor cells to the blood and directs them to adhere to and migrate into the damaged organ. Thus, these progenitor cells most likely constitute a natural repair mechanism that counteracts degenerative or aging processes. On the basis of encouraging experimental data, first clinical trials have been established to demonstrate the safety and the feasibility of progenitor cell therapy in case of peripheral artery disease or myocardial infarction. Trials investigating injection of bone marrow or circulating progenitor cells into the coronary artery after an acute myocardial infarction not only demonstrates safety of the procedure but also gave hints toward efficacy. Nevertheless, these findings have to be validated by subsequent larger, prospective, randomized, controlled trials. There are also potential topics in nephrology, where modification of progenitor cell activity might be of benefit, such as renal ischemic disease, glomerular disease, and renal transplant vasculopathy. Finding a way to integrate the principle of progenitor cell action into therapeutic efforts might provide a completely new therapeutic strategy that not only attempts to retard disease progression but furthermore targets to regenerate damaged organs.
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