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J Thorac Cardiovasc Surg 2008;135:986-990
© 2008 The American Association for Thoracic Surgery

Editorial

Cell therapy in ischemic settings: Fact and fiction

Gino Gerosa, MD*, Chiara d'Agostino, MD

Department Cardiac, Thoracic, and Vascular Sciences, Cardiac Surgery Section, University of Padova Medical School, Padova, Italy

Received for publication November 6, 2007; accepted for publication December 14, 2007.

* Address for reprints: Gino Gerosa, MD, University of Padova Medical School, Cardiac Surgery Unit, Cardiologic, Thoracic, and Vascular Science, Via Giustiniani 1, 35128 Padova, Italy. (Email: gino.gerosa@unipd.it).

The first 300 words of the full text of this article appear below.

Until the 1990s, it had always been thought that the adult heart could not renew its cells and that the number of cells present at birth would "dictate the destiny" of this organ through a person's life.1Go According to this idea, myocyte turnover did not occur, and cells formed during the embryonic and fetal life were responsible for the preservation of the heart until the end.

Apoptosis, according to this hypothesis, should not occur. The heart would rapidly lose a number of myocytes, and the remaining cells would not be able to support ventricular function.

The dogma was therefore that the heart cannot regenerate. Anversa challenged this assumption, leading to a "paradigm shift" in cardiac biology.2Go

The Expectations

Since Anversa showed that cardiomyocytes undergo apoptosis at a certain rate, the idea of the heart switched from a "still-life organ" to a self-renewing organ in which myocyte regeneration occurs. The injured heart may potentially act as a trigger for regenerative function; the process of repairing the damaged heart is thought to be related to the balance between regeneration and loss of myocytes. This was further confirmed recently with highly advanced mouse genetic engineering technologies allowing cellular tracking with a "fate mapping" approach.3Go This technique clearly confirmed that endogenous stem cells refresh adult mammalian cardiomyocytes after myocardial infarction or pressure overload. Although an increased number of mitotic cardiomyocytes and cardiac stem cells in the infarcted heart will accelerate the regeneration of new myocardium, an excessive loss of cardiomyocytes may also be induced by the ventricular mechanical stress and altered milieu in the infarcted heart. Because the number of mitotic cardiomyocytes in human beings is very low, a negative balance between regeneration and loss of myocytes might provide a reasonable explanation as to why self-repair of the damaged heart is not seen clinically. In line . . . [Full Text of this Article]






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