Abstract
It has become apparent over the past few decades that several factors can determine lethal or sublethal alterations of cardiovascular system cell function such as inflammatory reaction products, peptides and hormones. In turn, the loss of cellular components from the blood vessels wall and the heart tissue contributes to the development of cardiovascular diseases (CVD). Hence, in the recent years, the efforts of several research groups have specifically been devoted to deeply investigate the implication of the main forms of cell injury, necrosis, apoptosis and autophagy, in the development of cardiac and blood vessel alterations associated with human diseases. Furthermore, several lines of evidence demonstrate that CVD clearly display significant gender differences in terms of onset, progression and outcome. Cardiovascular cells contain functional estrogen and androgen receptors and are targets for sex hormone action, which can influence many physiological and pathological processes, including vascular and myocardial cell homeostasis. However, hormones are important but not unique actors in this issue, further genetic and epigenetic determinants being involved. This review focuses on recent studies on the effects of gender differences, including sex hormones, on cardiac and vascular cell injury and death and their influence in determining atherosclerosis, heart failure and other main human CVD.
Keywords: Gender, cell death, apoptosis, cardiovascular, sex hormones, cardiomyocytes, endothelial cells, vascular smooth muscle cells, lethal, implication, necrosis, autophagy, epigenetic, hypertension, vasculopathy, cathepsins, myocarditis, extravasation, autophagosomes, abrogation, Depolarization, cytoprotective
Current Pharmaceutical Design
Title: Gender Specific Aspects of Cell Death in the Cardiovascular System
Volume: 17 Issue: 11
Author(s): Marina Pierdominici, Elena Ortona, Flavia Franconi, Massimiliano Caprio, Elisabetta Straface and Walter Malorni
Affiliation:
Keywords: Gender, cell death, apoptosis, cardiovascular, sex hormones, cardiomyocytes, endothelial cells, vascular smooth muscle cells, lethal, implication, necrosis, autophagy, epigenetic, hypertension, vasculopathy, cathepsins, myocarditis, extravasation, autophagosomes, abrogation, Depolarization, cytoprotective
Abstract: It has become apparent over the past few decades that several factors can determine lethal or sublethal alterations of cardiovascular system cell function such as inflammatory reaction products, peptides and hormones. In turn, the loss of cellular components from the blood vessels wall and the heart tissue contributes to the development of cardiovascular diseases (CVD). Hence, in the recent years, the efforts of several research groups have specifically been devoted to deeply investigate the implication of the main forms of cell injury, necrosis, apoptosis and autophagy, in the development of cardiac and blood vessel alterations associated with human diseases. Furthermore, several lines of evidence demonstrate that CVD clearly display significant gender differences in terms of onset, progression and outcome. Cardiovascular cells contain functional estrogen and androgen receptors and are targets for sex hormone action, which can influence many physiological and pathological processes, including vascular and myocardial cell homeostasis. However, hormones are important but not unique actors in this issue, further genetic and epigenetic determinants being involved. This review focuses on recent studies on the effects of gender differences, including sex hormones, on cardiac and vascular cell injury and death and their influence in determining atherosclerosis, heart failure and other main human CVD.
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Cite this article as:
Pierdominici Marina, Ortona Elena, Franconi Flavia, Caprio Massimiliano, Straface Elisabetta and Malorni Walter, Gender Specific Aspects of Cell Death in the Cardiovascular System, Current Pharmaceutical Design 2011; 17 (11) . https://dx.doi.org/10.2174/138161211795656891
DOI https://dx.doi.org/10.2174/138161211795656891 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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