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Titlebook: Cardiac Energy Metabolism in Health and Disease; Gary D. Lopaschuk,Naranjan S. Dhalla Book 2014 Springer Science+Business Media New York 2

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樓主: ARGOT
11#
發(fā)表于 2025-3-23 12:47:16 | 只看該作者
Fuel Metabolism Plasticity in Pathological Cardiac Hypertrophy and Failurevelopment of pathological cardiac hypertrophy, a significant remodeling of metabolic pathways leads to a disruption in energy homeostasis, which contributes to the eventual heart failure. These changes include a shift of substrate preference from fatty acids to glucose, a reduction in the overall ox
12#
發(fā)表于 2025-3-23 16:27:45 | 只看該作者
13#
發(fā)表于 2025-3-23 20:11:10 | 只看該作者
The Role of AMPK in the Control of Cardiac Hypertrophyat can have profound detrimental consequences. AMP-activated protein kinase (AMPK), a well-studied mediator of cellular energy homeostasis, has been shown to be a regulator of cardiac hypertrophy via its influence on several key signaling pathways involved in cardiomyocyte growth control. Although t
14#
發(fā)表于 2025-3-24 01:20:39 | 只看該作者
15#
發(fā)表于 2025-3-24 06:05:39 | 只看該作者
Metabolic Therapy for the Ischemic Heart flow limiting coronary stenosis is the main recognized pathological mechanism underlying this condition. While revascularization procedures are performed with the aim to remove the flow limiting stenosis, traditional medical therapy with hemodynamic agents aim at reducing oxygen demand of the myoca
16#
發(fā)表于 2025-3-24 07:37:51 | 只看該作者
Inhibition of Fatty Acid Oxidation to Treat Heart Failure in Patientsaltered in heart failure and has been considered a contributing factor in the impaired heart function observed in patients with heart failure. Emerging evidence demonstrates that correcting these changes in energy metabolism by modulating mitochondrial oxidative metabolism may be effective treatment
17#
發(fā)表于 2025-3-24 14:19:40 | 只看該作者
18#
發(fā)表于 2025-3-24 18:03:56 | 只看該作者
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發(fā)表于 2025-3-24 21:11:50 | 只看該作者
20#
發(fā)表于 2025-3-25 02:48:45 | 只看該作者
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