Activation of Apoptotic Caspase Cascade During the Transition to Pressure Overload-Induced Heart Failure
نویسندگان
چکیده
منابع مشابه
Activation of apoptotic caspase cascade during the transition to pressure overload-induced heart failure.
OBJECTIVES A pressure overload model was developed to simulate aortic stenosis and assess caspase activity during the transition to heart failure. BACKGROUND Cardiomyocyte apoptosis is implicated in the pathogenesis of heart failure, and caspase activation is central to this pathophysiological process. METHODS A total of 10 sheep were banded with variable aortic constriction devices, progre...
متن کاملCD4+ T cells promote the transition from hypertrophy to heart failure during chronic pressure overload.
BACKGROUND The mechanisms by which the heart adapts to chronic pressure overload, producing compensated hypertrophy and eventually heart failure (HF), are still not well defined. We aimed to investigate the involvement of T cells in the progression to HF using a transverse aortic constriction (TAC) model. METHODS AND RESULTS Chronic HF was associated with accumulation of T lymphocytes and act...
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Changes in oxidative stress and apoptotic process were studied during the progression of a compensated hypertrophy to a decompensated heart failure in guinea pigs. Banding of the ascending aorta resulted in heart hypertrophy. At 10 wk, ventricle-to-body weight ratio and thickness of the interventricular septum as well as the left ventricular wall were increased significantly. Although fractiona...
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Rescue of Pressure Overload-Induced Heart Failure by Estrogen Therapy.
BACKGROUND Estrogen pretreatment has been shown to attenuate the development of heart hypertrophy, but it is not known whether estrogen could also rescue heart failure (HF). Furthermore, the heart has all the machinery to locally biosynthesize estrogen via aromatase, but the role of local cardiac estrogen synthesis in HF has not yet been studied. Here we hypothesized that cardiac estrogen is re...
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ژورنال
عنوان ژورنال: Journal of the American College of Cardiology
سال: 2006
ISSN: 0735-1097
DOI: 10.1016/j.jacc.2006.05.065