Estrogens and the prevention of cardiac apoptosis
A large array of cardiac diseases such as hypertensive heart disease and cardiac remodeling after myocardial infarction display significant gender-based differences (1, 2, 3). In this context it has been shown that during the process of aging cardiac number and diameter vary significantly between men and women. While cardiac myocytes of male patients tend to develop hypertrophy and polyploidy, cardiac myocytes of female patients remain consistent over time in terms of size and number of nuclei (4). The underlying mechanisms of this process remain to be elucidated. However, it is remarkable that the incidence of cardiac disease in female gender reveals a significant increase after the onset of menopause (5). Therefore it has been hypothesized that the decline of ovarian sex hormones after the onset of menopause, in particular estrogens, play an important role in the pathogenesis of cardiac disease in women. The role of estrogen in the pathogenesis of this process is currently under investigation (6–11). The influence of estrogen on the development of cardiac diseases can be divided in systemic and direct effects on the cardiovascular system. Systemic effects include the influence of sex hormones on lipid and insulin metabolism (12, 13). Furthermore, it has become evident that estrogens display a variety of genomic and non-genomic effects on cardiovascular tissues that may modulate the respective phenotype of these tissues. Two different estrogen receptors have been identified so far, estrogen receptor α and estrogen receptor β. These two subtypes differ in ligand binding as well as in DNA binding properties (14-18).
KeywordsEstrogen Receptor Hypertensive Heart Disease Ovariectomized Animal Estrogen Withdrawal Left Ventricular Tissue
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