作者: S. Mahmoodzadeh , D. Fliegner , E. Dworatzek
DOI: 10.1007/978-3-642-30726-3_2
关键词: Heart failure 、 Pressure overload 、 Bioinformatics 、 Heart disease 、 Estrogen 、 Sexual dimorphism 、 Animal studies 、 Muscle hypertrophy 、 Endocrinology 、 Internal medicine 、 Sex hormone-binding globulin 、 Medicine
摘要: Clinical findings show sex differences in the manifestation of a number cardiovascular diseases (CVD). However, underlying molecular mechanisms are incompletely understood. Multiple animal models suggest CVD, and provide strong experimental evidence that different major pathways regulated sex-specific manner. In most studies females display lower mortality, less severe hypertrophy, better preserved cardiac function compared with male counterparts. The data support hypothesis female and/or hormone estrogen (17β-estradiol; E2) may contribute to sexual dimorphism heart outcome females. To improve our understanding sex-based cellular CVD develop new therapeutic strategies, use appropriate is essential. This review highlights recent from relevant for studying dimorphisms healthy diseased heart, focusing on physiological hypertrophy (exercise), pathological (volume pressure overload induced hypertrophy), failure (myocardial infarction). Furthermore, potential effects E2 these will be discussed.