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Abstract

Cardiac myocytes are terminally differentiated cells with distinct electrical and mechanical characteristics that exhibit a high degree of functional specialization. Although some controversy exists, they are generally considered to be post-mitotic, having lost their regenerative capacity [4, 65]. On the other hand, loss of cardiac myocytes is a pathologic feature of several cardiac disease states among which massive necrosis of myocardial tissue is the one that comes to mind first. However, in recent years increasing evidence has accumulated that myocyte loss by apoptosis may also contribute to the pathophysiology of myocardial disease [25]. Among others apoptosis was detected in acute ischemia and reperfusion, chronic heart failure due to dilated cardiomyopathy and ischemic heart disease, and myocardial hypertrophy due to increased afterload. This, in conjunction with the fact that the number of cardiac myocytes is a critical determinant for cardiac function, has increased the interest of cardiovascular researchers in defining the mechanisms and potentials of a treatment strategy aimed at inhibiting apoptotic myocyte loss. Based on current knowledge about myocyte apoptosis, apoptotic mechanisms that may be targeted to prevent myocyte apoptosis will be delineated (Fig. 1). Both inhibition of pro-apoptotic pathways and promotion of anti-apoptotic mechanisms will be considered in more detail. In addition, potential problems inherent to an anti-apoptotic treatment approach are also discussed.

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Haunstetter, A., Izumo, S. (2000). Strategies to prevent apoptosis. In: Hasenfuss, G., Marbán, E. (eds) Molecular Approaches to Heart Failure Therapy. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-642-57710-9_16

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  • DOI: https://doi.org/10.1007/978-3-642-57710-9_16

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