Effects of Ubiquinol in Reducing the Development of Heart Failurewith Preserved Ejection Fraction and Mitochondrial Injury
@article{Shen2016EffectsOU, title={Effects of Ubiquinol in Reducing the Development of Heart Failurewith Preserved Ejection Fraction and Mitochondrial Injury}, author={Qiuhua Shen and John B. Hiebert and Amanda R Thimmesch and Richard L. Clancy and Janet D. Pierce}, journal={Research and reviews: journal of nursing and health sciences}, year={2016}, volume={2} }
There is currently no effective clinical treatment for diastolic heart failure also termed heart failure with preserved ejection fraction (HFpEF) which is associated with reduced myocardial adenosine triphosphate. Ubiquinol in the electron chain is required for adenosine triphosphate synthesis. Thus, the purpose of this pilot study was to examine in a rat model the effects of ubiquinol (reduced form of Coenzyme Q10) in the development of HFpEF. Six Dahl salt-sensitive rats were randomly…
References
SHOWING 1-10 OF 40 REFERENCES
Myocardial energetics and ubiquinol in diastolic heart failure.
- MedicineNursing & health sciences
- 2014
Clinicians and health scientists should be aware of the potential role of this supplement, ubiquinol, which is an antioxidant and is required for adenosine triphosphate production, in the treatment of diastolic heart failure.
Coenzyme Q10: an independent predictor of mortality in chronic heart failure.
- MedicineJournal of the American College of Cardiology
- 2008
Mitochondrial energy conversion disturbance with decrease in ATP production as a source of systemic arterial hypertension.
- Biology, MedicinePathophysiology : the official journal of the International Society for Pathophysiology
- 2007
The cause of stationary elevated BP in chronic arterial hypertension should be regarded as a compensatory response to decreased mitochondrial ATP synthesis, which results in the long-term maintenance of elevated BP by increased sympathetic outflow and augmented ROS production following mitochondrial dysfunction.
Redox-sensitive mechanisms underlying vascular dysfunction in heart failure
- BiologyFree radical research
- 2015
The sources of ROS in the vasculature are summarized, the impact of oxidative stress on functional and structural vascular remodeling is elucidated, and the importance of vascular dysfunction in HF is pointed out and therapeutic options are discussed.
Interplay of defective excitation-contraction coupling, energy starvation, and oxidative stress in heart failure.
- BiologyTrends in cardiovascular medicine
- 2011
Novel aspects of ROS signalling in heart failure
- BiologyBasic Research in Cardiology
- 2013
Current understanding of the roles of redox signalling pathways in the pathophysiology of heart failure, including effects on cardiomyocyte hypertrophy signalling, excitation–contraction coupling, arrhythmia, cell viability and energetics are reviewed.
Mitochondrial calcium overload is a key determinant in heart failure
- BiologyProceedings of the National Academy of Sciences
- 2015
It is shown for the first time, to the authors' knowledge, that diastolic SR Ca2+ leak causes mitochondrial Ca2- overload and dysfunction in a murine model of postmyocardial infarction HF.
Mechanisms of diastolic dysfunction in heart failure.
- MedicineTrends in cardiovascular medicine
- 2006
Effects of ubiquinol with fluid resuscitation following haemorrhagic shock on rat lungs, diaphragm, heart and kidneys
- MedicineExperimental physiology
- 2014
The administration of ubiquinol attenuated damage to the lungs, diaphragm, heart and kidneys following haemorrhagic shock and fluid resuscitation, suggesting that ubiquinols could be a potential antioxidant used to reduce the reperfusion injury following haemsorrhaging shock.
Biochemical, physiological and medical aspects of ubiquinone function.
- Biology, ChemistryBiochimica et biophysica acta
- 1995