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Cardiovascular Research 2003 59(3):549-562; doi:10.1016/S0008-6363(03)00498-X
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Cardiomyocyte apoptosis in hypertensive cardiomyopathy

Arantxa Gonzáleza, María A Fortuñoa, Ramón Querejetab, Susana Ravassaa, Begoña Lópeza, Natalia Lópeza and Javier Díeza,c,*

aDivision of Cardiovascular Pathophysiology, Centre for Applied Medical Research, School of Medicine, University of Navarra, Pamplona, Spain
bDonostia University Hospital, San Sebastián, Spain
cDepartment of Cardiology and Cardiovascular Surgery, University Clinic, School of Medicine, University of Navarra, Pamplona, Spain

jadimar{at}unav.es

* Corresponding author. División de Fisiopatología Cardiovascular, Facultad de Medicina, Universidad de Navarra, C/Irunlarrea 1, 31080 Pamplona, Spain. Tel.: +34-948-425-600; fax: 34-948-425-649.

It is widely accepted that there are two principal forms of cell death; namely, necrosis and apoptosis. According to the classical view, necrosis is the major mechanism of cardiomyocyte death in cardiac diseases. However, in the past few years observations have been made showing that cardiomyocyte apoptosis occurs in diverse conditions and that apoptosis may be a contributing cause of the loss and functional abnormalities of cardiomyocytes with important pathophysiological consequences. In this regard, although a number of formal proofs are pending, it is conceivable that cardiomyocyte apoptosis may be an important variable in the clinical evolution of hypertensive cardiomyopathy. This review summarizes recent evidence demonstrating that cardiomyocyte apoptosis is abnormally stimulated in the heart of animals and humans with arterial hypertension. In addition, the potential mechanisms of cardiomyocyte apoptosis in hypertension and its detrimental impact on cardiac function will be addressed. Finally, the perspectives of strategies aimed to detect and modulate apoptosis of cardiomyocytes in hypertensive cardiomyopathy will be considered.

KEYWORDS Apoptosis; Arterial hypertension; Cardiomyocytes; Heart failure


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