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AMPK: a therapeutic target of heart failure - not only metabolism regulation

Published on Jan 31, 2019in Bioscience Reports2.535
· DOI :10.1042/BSR20181767
Xuan Li3
Estimated H-index: 3
(UMMC: University of Mississippi Medical Center),
Jia Liu3
Estimated H-index: 3
(UMMC: University of Mississippi Medical Center)
+ 5 AuthorsJi Li34
Estimated H-index: 34
(UMMC: University of Mississippi Medical Center)
Abstract
Heart failure (HF) is a serious disease with high mortality. The incidence of this disease has continued to increase over the past decade. All cardiovascular diseases causing dysfunction of various physiological processes can result in HF. AMP-activated protein kinase (AMPK), an energy sensor, has pleiotropic cardioprotective effects and plays a critical role in the progression of HF. In this review, we highlight that AMPK can not only improve the energy supply in the failing heart by promoting ATP production, but can also regulate several important physiological processes to restore heart function. In addition, we discuss some aspects of some potential clinical drugs which have effects on AMPK activation and may have value in treating HF. More studies, especially clinical trials, should be done to evaluate manipulation of AMPK activation as a potential means of treating HF.
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  • Citations (3)
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References126
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#1Xuan Li (UMMC: University of Mississippi Medical Center)H-Index: 3
#2Jia Liu (UMMC: University of Mississippi Medical Center)H-Index: 3
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Abstract Background AMP-activated Protein Kinase (AMPK) is a stress-activated kinase that protects against cardiomyocyte injury during ischemia and reperfusion. c-Jun N-terminal kinase (JNK), a mitogen activated protein kinase, is activated by ischemia and reperfusion. NF-κB is an important transcription factor involved in ischemia and reperfusion injury. Methods and Results The intrinsic activation of AMPK attenuates the inflammation which occurred during ischemia/reperfusion through the modula...
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#2Nanhu Quan (UMMC: University of Mississippi Medical Center)H-Index: 7
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#2Kai Li (WMU: Weifang Medical University)H-Index: 1
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Perivascular adipose tissue (PVAT) loses its anti-contractile activity in obesity. Calycosin, the major bioactive isoflavonoid, was shown to protect endothelial function. However, effects of calycosin on PVAT function in obesity remain unclear. We aimed to investigate the effects of calycosin on the anti-contractile activity of PVAT in obese mice and its potential mechanisms. Obesity in mice was induced with a high-fat diet, with or without calycosin treatment. Thoracic aorta responses to phenyl...
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