Metabolic remodelling of the failing heart: the cardiac burn-out syndrome?
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منابع مشابه
Metabolic remodelling of the failing heart: the cardiac burn-out syndrome?
It has been postulated that the failing heart suffers from chronic energy starvation, and that derangements in cardiac energy conversion are accessory to the progressive nature of this disease. The molecular mechanisms driving this 'metabolic remodelling' process and their significance for the development of cardiac failure are still open to discussion. Next to changes in mitochondrial function...
متن کاملMetabolic remodelling of the failing heart: beneficial or detrimental?
The failing heart is characterized by alterations in energy metabolism, including mitochondrial dysfunction and a reduction in fatty acid (FA) oxidation rate, which is partially compensated by an increase in glucose utilization. Together, these changes lead to an impaired capacity to convert chemical energy into mechanical work. This has led to the concept that supporting cardiac energy convers...
متن کاملHMGB1 Attenuates Cardiac Remodelling in the Failing Heart via Enhanced Cardiac Regeneration and miR-206-Mediated Inhibition of TIMP-3
AIMS HMGB1 injection into the mouse heart, acutely after myocardial infarction (MI), improves left ventricular (LV) function and prevents remodeling. Here, we examined the effect of HMGB1 in chronically failing hearts. METHODS AND RESULTS Adult C57 BL16 female mice underwent coronary artery ligation; three weeks later 200 ng HMGB1 or denatured HMGB1 (control) were injected in the peri-infarct...
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The pathophysiology of heart failure (HF) has long been linked to a neurohormonal imbalance because of excessive compensatory activation of the sympathetic nervous system (SNS). As HF develops, cardiac function is progressively lost prompting an increase in SNS activity in an attempt to maintain homeostasis and stabilize cardiac output. Although initially providing beneficial ionotropic support...
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ژورنال
عنوان ژورنال: Cardiovascular Research
سال: 2004
ISSN: 0008-6363
DOI: 10.1016/j.cardiores.2003.11.014