Cardiomyocyte apoptosis is related to left ventricular dysfunction and remodelling in dilated cardiomyopathy, but is not affected by growth hormone treatment-Reference-Cited by-同舟云学术

Cardiomyocyte apoptosis is related to left ventricular dysfunction and remodelling in dilated cardiomyopathy, but is not affected by growth hormone treatment

Published:2007-02 Issue:2 Volume:9 Page:160-167
ISSN:1388-9842
Container-title:European Journal of Heart Failure
language:en
Short-container-title:European Journal of Heart Failure

Author:

Ibe Waltraut¹,Saraste Antti²,Lindemann Stephan³,Bruder Stephanie⁴,Buerke Michael⁵,Darius Harald⁶,Pulkki Kari⁷,Voipio-Pulkki Liisa-Maria⁸

Affiliation:

1. Department of Cardiology; Suedharz-Hospital; Robert-Koch-Strasse 39 99734 Nordhausen Germany

2. Department of Anatomy; University of Turku; Kiinamyllynkatu 10 20520 Turku Finland

3. Department of Cardiology; University of Tübingen; Otfried-Müller-Strasse 10 72076 Tübingen Germany

4. Department of Cardiology; University of Mainz; Langenbeckstrasse 1 55101 Mainz Germany

5. Department of Cardiology; University of Halle-Wittenberg; Universitätsplatz 10 06108 Halle/Saale Germany

6. Department of Cardiology; Vivantes Hospital Neukölln; Rudowerstrasse 48 12351 Berlin Germany

7. Department of Laboratory Diagnostics; Helsinki University Central Hospital; POB 340 00029 Helsinki Finland

8. Department of Medicine; Helsinki University Central Hospital; POB 340 00029 Helsinki Finland

Publisher

Wiley

Subject

Cardiology and Cardiovascular Medicine

Reference42 articles.

1. Apoptosis in myocytes in end-stage heart failure;Narula;N Engl J Med,1996

2. Apoptosis in the failing human heart;Olivetti;N Engl J Med,1997

3. Myocytes die by multiple mechanisms in failing human hearts;Kostin;Circulation,2003

4. Cardiomyocyte apoptosis and progression of heart failure to transplantation;Saraste;Eur J Clin Invest,1999

5. Inhibition of cardiac myocyte apoptosis improves cardiac function and abolishes mortality in the peripartum cardiomyopathy of Galphaq transgenic mice;Hayakawa;Circulation,2003

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