In patients with chronic heart failure (CHF), the addition of coenzyme Q10 to conventional therapy reduces the hospitalization rate for worsening of heart failure and the incidence of serious cardiovascular complications. The present study was planned to assess the hemodynamic mechanisms underlying this phenomenon. Cardiac hemodynamics was evaluated continuously using an ambulatory radionuclide detector (VEST) which allows a noninvasive monitoring of left ventricular function. Six patients wit CHF (mean ejection fraction (EF): 29%) clinically documented were studied. This study was organized as a randomized double-blind, placebo controlled, cross-over trial. The enrolled patients, after a washout period, underwent the first hemodynamic evaluation with VEST. Subsequently they were randomized to receive placebo or coenzyme Q10 for 4 weeks. At the end of this period they underwent the second VEST study. The third VEST study was performed after a further 4-week period with inverted treatment. Cardiac hemodynamics were evaluated during bicycle exercise. The EF in control conditions (CC) changed from 27 +/- 11%, at rest, to 24 +/- 8%, at peak exercise. During coenzyme Q10 treatment EF showed a significant increase both at rest (33 +/- 13%, P < 0.05 vs CC) and at peak exercise (30 +/- 12%, P < 0.05 vs CC). The same trends were recorded for the stroke volume and the cardiac output. Our results demonstrate that coenzyme Q10 improves cardiac hemodynamic response to exercise in patients with CHF and suggest that noninvasive monitoring of left ventricular function allows a more reliable assessment of therapy efficacy.
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http://dx.doi.org/10.1016/0098-2997(94)90025-6 | DOI Listing |
Front Neurosci
January 2025
Department of Geriatric Rehabilitation, Jiangbin Hospital, Nanning, China.
Background: Programmed cell death plays an important role in neuronal injury and death after ischemic stroke (IS), leading to cellular glucose deficiency. Glucose deficiency can cause abnormal accumulation of cytotoxic disulfides, resulting in disulfidptosis. Ferroptosis, apoptosis, necroptosis, and autophagy inhibitors cannot inhibit this novel programmed cell death mechanism.
View Article and Find Full Text PDFIran J Basic Med Sci
January 2025
Molecular Medicine Research Center, Biomedicine Institute, Tabriz University of Medical Sciences, Tabriz, Iran.
Objectives: Ischemia/reperfusion (IR)-induced ventricular arrhythmia, which mainly occurs after the opening of coronary artery occlusion, poses a clinical problem. This study aims to investigate the effectiveness of pretreatment with coenzyme Q (CoQ) in combination with mitochondrial transplantation on IR-induced ventricular arrhythmias in aged rats.
Materials And Methods: Myocardial IR induction was performed by left anterior descending coronary artery occlusion for 30 min, followed by re-opening for 24 hr.
Front Pediatr
January 2025
Department of Pediatric Nephrology, Children's Hospital of Hebei Province Affiliated to Hebei Medical University, Shijiazhuang, China.
Background: Primary coenzyme Q10 (CoQ10) deficiency is an autosomal recessive genetic disease caused by mitochondrial dysfunction. Variants in Coenzyme Q8B () can cause primary CoQ10 deficiency. -related glomerulopathy is a recently recognized glomerular disease that most often presents as steroid-resistant nephrotic syndrome (SRNS) in childhood.
View Article and Find Full Text PDFMol Oncol
January 2025
Division of Cancer Cell Biology, Department of Pharmaceutical Sciences, Showa University Graduate School of Pharmacy, Tokyo, Japan.
The role of the electron transport chain (ETC) in cell proliferation control beyond its crucial function in supporting ATP generation has recently emerged. In this study, we found that, among the four ETC complexes, the complex I (CI)-mediated NAD regeneration is important for cancer cell proliferation. In cancer cells, a decrease in CI activity by RNA interference (RNAi) against NADH:ubiquinone oxidoreductase core subunit V1 (NDUFV1) arrested the cell cycle at the G/S phase, accompanying upregulation of p21 cyclin-dependent kinase inhibitor expression.
View Article and Find Full Text PDFBackground: Atherosclerosis (AS) is caused by the endothelium injury associated with oxidative stress. Previous studies have shown that the Phlegm-Eliminating and Stasis- Transforming Decoction (Huayu Qutan Decoction, HYQTD) has mitochondrial protective function. The objective of this research was to explore how HYQTD drug-containing serum (HYQTD-DS) could potentially protect mitochondrial energy production in endothelial cells (ECs) from injury caused by hydrogen peroxide (H2O2)-induced oxidative damage in AS through SIRT1/PGC-1α/ Nrf2 pathway.
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