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Circulation Research. 2005;96:6-8
doi: 10.1161/01.RES.0000153667.26414.10
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(Circulation Research. 2005;96:6.)
© 2005 American Heart Association, Inc.


Editorials

Bone Marrow Stem Cells for Myocardial Infarction

Effector or Mediator?

Florian P. Limbourg, Helmut Drexler

From the Hannover Medical School, Department of Cardiology and Angiology, Hannover, Germany.

Correspondence to Helmut Drexler, Hannover Medical School, Dept of Cardiology and Angiology, Carl-Neubergstr. 1, 30625 Hannover, Germany. E-mail Drexler.Helmut@MH-Hannover.de


Key Words: bone marrow stem cells • myocardial regeneration • transdifferentiation • myocardial infarction • cell fusion


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

I’ll be back!

— —Arnold Schwarzenegger

When news broke in 2001 that bone marrow–derived stem cells (BMCs) regenerate cardiac myocytes after myocardial infarction (MI), the prospects of regenerative therapy suddenly dawned on the horizon of cardiovascular medicine. Along with reports about differentiation of BMCs into neurons, hepatocytes, and muscle,1–4 BMCs delivered to the heart were shown to transdifferentiate into cardiac myocytes and to rescue cardiac function after infarction.5,6 In fact, the initial reports by Anversa’s group,5,6 supported by numerous similar findings, spurred the translation of stem cell therapy into the clinical arena, although the cell isolation and delivery strategies for patients with acute MI differed considerably from the experimental procedures of direct myocardial injection. Indeed, a number of clinical trials now suggest not only safety and feasibility of stem cell therapy but also significant improvement of left ventricular function in patients with acute myocardial infarction.7–10

However, the ability of BMCs to transdifferentiate into cardiac myocytes has recently been questioned by various groups that failed to demonstrate permanent engraftment of transplanted BMCs in the infarcted heart. Because improvements in cardiac function were still noted despite the lack of myocyte transdifferentiation, alternate mechanisms of BMC action have been suggested to support cardiac recovery.11–13 Accompanying editorials questioned the methodological approach by Anversa’s group and the early translation of "controversial findings" into clinical trials.14 After all this heat, Anversa’s group was tuned "to be back" (like the Terminator). In this issue of Circulation Research, Kajstura et al15 add new fuel to the stem . . . [Full Text of this Article]


Related Article:

Bone Marrow Cells Differentiate in Cardiac Cell Lineages After Infarction Independently of Cell Fusion
Jan Kajstura, Marcello Rota, Brian Whang, Stefano Cascapera, Toru Hosoda, Claudia Bearzi, Daria Nurzynska, Hideko Kasahara, Elias Zias, Massimiliano Bonafé, Bernardo Nadal-Ginard, Daniele Torella, Angelo Nascimbene, Federico Quaini, Konrad Urbanek, Annarosa Leri, and Piero Anversa
Circ. Res. 2005 96: 127-137. [Abstract] [Full Text] [PDF]



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