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DNA(Cohen 1997; Saikumar et al. 1999). The activation of BAX is counteracted by the
action of the members of Bcl-2 anti apoptotic group of proteins.
III.b. Apoptosis and heart failure
Heart failure is considered to be a final common pathway of diverse etiologies
and is characteized by the impairment of systolic and/or diastolic function causing the
hypo-perfusion of peripheral organs. One of most important characteristic of heart failure
is a loss of myocytes. Because of the fact that cardiac myocytes are terminally
differentiated cells, the loss of myocytes will compromise the hemodlmamic function of
the heart leading to the signs of heart failure. Traditionally, the loss of myocytes is
attributed to the development of necrosis. However, over the last few decades, a new
concept is emerging implicating the role of apoptosis in the pathogenesis of heart failure
(Van Empel et a. 2005; Garg et al. 2005). The initial evidence supporting the role of
apoptosis in congestive heart failure was obtained by a number of studies that have
positively identified the occurrence of apoptosis in endomyocardial biopsy specimens
obtained from the patients suffering from a dilated and ischemic cardiomyopathy. The
occuffence of apoptosis was also confirmed in the failing hearts that were explanted from
the patients undergoing cardiac transplantation (Narula et al. 1996; Olivetti et al. 1997).
A number of studies using experimental models of heart failure due to different
etiologies such as; ischemia-reperfusion, hypoxia, calcium excess, oxidative sttess, gene
induction, rapid pacing, stretching of myocytes and adriamycin-administration strongly
support a notion that apoptosis is involved in the pathogenesis of heart failure (Cheng et
al. 1995; Gottlieb et al. 1994; Hamet et al. T995; Kajstura et aL 1996; Liu et al. 1995;
Sharov etal.1996; Thompson 1995).
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