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Cardiovascular Research 2003 59(2):268-270; doi:10.1016/S0008-6363(03)00480-2
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Ischemia/reperfusion-induced apoptosis: connecting nitric oxide and cell cycle regulators

Carla Pignatti and Claudio Stefanelli*

Department of Biochemistry "G. Moruzzi", University of Bologna, Via Irnerio, 48, 40126 Bologna, Italy

* Corresponding author. Tel.: +39-51-2091203; fax: +39-51-2091224. claudio.stefanelli@unibo.it

The first 150 words of the full text of this article appear below.

See article by Maejima et al. [1] (pages 308–320) in this issue.

Cardiomyocytes are able to divide throughout the fetal period of life and continue to increase in cell number up to the first 2-3 days after birth. Thereafter, they undergo terminal differentiation. Although in certain pathological conditions, such as myocardial infarction, cardiomyocyte proliferation has been observed also in the adult heart [2], postnatal cardiomyocytes are normally irreversibly withdrawn from the cell cycle, resulting in the loss of their regenerative capacity. In response to some stimuli, such as increased overload and ischemia, cardiac myocytes can grow by hypertrophy, which is accompanied by the upregulation of protein synthesis [3]. Hypertrophic and mitogenic stimuli share similar intracellular responses, such as multiple second messenger systems and induction of various immediate-early genes. Actually, serum stimulation of neonatal, terminally-differentiated cardiomyocytes, similarly to what happens in proliferating cells, upregulates some of the cell cycle . . . [Full Text of this Article]


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