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Inhibition of cardiac myocyte apoptosis by gp130-dependent cytokines

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Book cover Apoptosis in Cardiac Biology

Part of the book series: Basic Science for the Cardiologist ((BASC,volume 5))

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Abstract

In animal models and in patients with end-stage heart failure, a small fraction of cardiac myocytes undergoes programmed cell death (apoptosis) (1–4). In general, cardiac failure is preceded by a hypertrophic response of the myocardium, that allows the heart to maintain cardiac output despite a chronic increase in hemodynamic load. However, sustained hemodynamic overloading eventually causes a transition from hypertrophy to heart failure, characterized by chamber dilatation, progressive contractile dysfunction and impaired survival. The observation that the prevalence of apoptotic cardiomyocytes is increased in the failing heart but not during the initial stage of compensatory hypertrophy has given rise to the hypothesis that cardiac myocyte dropout by apoptosis may be one mechanism contributing to the progression of cardiac hypertrophy to heart failure (5,6).

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  1. Medizinische Hochschule Hannover, Hannover, Germany

    Kai C. Wollert M.D.

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  1. University of Regensburg, Germany

    Heribert Schunkert  & G. A. J. Riegger  & 

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Wollert, K.C. (2000). Inhibition of cardiac myocyte apoptosis by gp130-dependent cytokines. In: Schunkert, H., Riegger, G.A.J. (eds) Apoptosis in Cardiac Biology. Basic Science for the Cardiologist, vol 5. Springer, Boston, MA. https://doi.org/10.1007/978-0-585-38143-5_6

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  • DOI: https://doi.org/10.1007/978-0-585-38143-5_6

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-7923-8648-3

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