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Estrogen Therapy Rescues Advanced He...
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Iorga, Andrea.
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Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta./
作者:
Iorga, Andrea.
面頁冊數:
173 p.
附註:
Source: Dissertation Abstracts International, Volume: 76-10(E), Section: B.
Contained By:
Dissertation Abstracts International76-10B(E).
標題:
Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3705606
ISBN:
9781321788297
Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta.
Iorga, Andrea.
Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta.
- 173 p.
Source: Dissertation Abstracts International, Volume: 76-10(E), Section: B.
Thesis (Ph.D.)--University of California, Los Angeles, 2015.
Cardiac hypertrophy, defined as an enlargement of the ventricles, is often triggered when the heart is subjected to hemodynamic stress from physiological stimuli such as pregnancy, or from pathological stimuli such as pressure overload-induced left ventricular hypertrophy or pulmonary hypertension-induced right ventricular hypertrophy. Physiological hypertrophy is beneficial and adaptive, while pathological hypertrophy is maladaptive and detrimental.
ISBN: 9781321788297Subjects--Topical Terms:
518431
Physiology.
Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta.
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Source: Dissertation Abstracts International, Volume: 76-10(E), Section: B.
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Adviser: Mansoureh Eghbali.
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Thesis (Ph.D.)--University of California, Los Angeles, 2015.
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Cardiac hypertrophy, defined as an enlargement of the ventricles, is often triggered when the heart is subjected to hemodynamic stress from physiological stimuli such as pregnancy, or from pathological stimuli such as pressure overload-induced left ventricular hypertrophy or pulmonary hypertension-induced right ventricular hypertrophy. Physiological hypertrophy is beneficial and adaptive, while pathological hypertrophy is maladaptive and detrimental.
520
$a
It is well documented that in pathological hypertrophy the proteasomal activity is greatly disrupted, but nothing was known about possible regulation of proteasome activity/expression in physiological hypertrophy. In chapter 2 I show that physiological hypertrophy is downregulated, with a concomitant decrease in protein ubiquitination and reactive oxygen production. These findings lead to the conclusion that during pregnancy, the levels of aberrant or misfolded proteins are decreased.
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Secondly, estrogen treatment prior to the onset of pathological stimuli is known to attenuate the progression of the onset of ventricular hypertrophy, cardiac dysfunction and subsequent failure. However it was not known whether estrogen is also effective in rescuing heart failure since heart failure is not often diagnosed early and therapeutic intervention after the onset of hypertrophy and failure is necessary. In Chapters 3 and 4 I use two different models of hypertrophy and failure, the pressure overload-induced left ventricular hypertrophy and failure as well as the pulmonary hypertension-induced right ventricular hypertrophy and failure. I show that short-term estrogen therapy after the onset of cardiac dysfunction in both models rescues function via activation of the estrogen receptor beta. This rescue action of estrogen is also associated with reversal of cardiac fibrosis and stimulation of angiogenesis, both of which are essential in nurturing the heart.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3705606
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