Clinical Evidence for Q10 Coenzyme Supplementation in Heart Failure: From Energetics to Functional Improvement

Lorenzo, Anna Di; Iannuzzo, Gabriella; Parlato, Alessandro; Cuomo, Gianluigi; Testa, Crescenzo; Coppola, Mariangela; D’Ambrosio, Giuseppe; Oliviero, Domenico Alessandro; Sarullo, Silvia; Vitale, Giuseppe; Nugara, Cinzia; Sarullo, Filippo M; Giallauria, Francesco

doi:10.3390/jcm9051266

Cited by 44 publications

(38 citation statements)

References 93 publications

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“…Coenzyme Q (CoQ) plays a crucial role in the production of mitochondrial energy and reactive oxygen. CoQ is considered to be an antioxidant, and lack of it can lead to an increase in mitochondrial reactive oxygen species [ 16 ]. This could suggest that AAAs have mitochondrial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Plasma Metabolomics Analysis Identifies Abnormal Energy, Lipid, and Amino Acid Metabolism in Abdominal Aortic Aneurysms

et al. 2020

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Background Abdominal aortic aneurysm (AAA) is a complicated aortic dilatation disease. Metabolomics is an emerging system biology method. This aim of this study was to identify abnormal metabolites and metabolic pathways associated with AAA and to discover potential biomarkers that could affect the size of AAAs. Material/Methods An untargeted metabolomic method was used to analyze the plasma metabolic profiles of 39 patients with AAAs and 30 controls. Multivariate analysis methods were used to perform differential metabolite screening and metabolic pathway analysis. Cluster analysis and univariate analysis were performed to identify potential metabolites that could affect the size of an AAA. Results Forty-five different metabolites were identified with an orthogonal projection to latent squares-discriminant analysis model and the differences between them in the patients with AAAs and the control group were compared. A variable importance in the projection score >1 and P<0.05 were considered statistically significant. In patients with AAAs, the pathways involving metabolism of alanine, aspartate, glutamate, D-glutamine, D-glutamic acid, arginine, and proline; tricarboxylic acid cycling; and biosynthesis of arginine are abnormal. The progression of an AAA may be related to 13 metabolites: citric acid, 2-oxoglutarate, succinic acid, coenzyme Q1, pyruvic acid, sphingosine-1-phosphate, platelet-activating factor, LysoPC (16: 00), lysophosphatidylcholine (18: 2(9Z,12Z)/0: 0), arginine, D-aspartic acid, and L- and D-glutamine. Conclusions An untargeted metabolomic analysis using ultraperformance liquid chromatography-tandem mass spectrometry identified metabolites that indicate disordered metabolism of energy, lipids, and amino acids in AAAs.

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Section: Discussionmentioning

confidence: 99%

Plasma Metabolomics Analysis Identifies Abnormal Energy, Lipid, and Amino Acid Metabolism in Abdominal Aortic Aneurysms

et al. 2020

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“…CoQ 10 deficiency is associated with several diseases, such as cardiovascular diseases, muscular dystrophy and neurodegenerative disorders ( 87 ). Administration of CoQ 10 as a supplement along with standard clinical therapy shows positive effects in patients with hypertension ( 87 ) and heart failure ( 89 ). Higher plasma CoQ 10 concentrations in patients with MI lead to improved left ventricular function.…”

Section: Current Developments In Mitochondria-targeted Agents Withmentioning

confidence: 99%

Mitochondria as a therapeutic target for cardiac ischemia‑reperfusion injury (Review)

Marin

et al. 2020

Int J Mol Med

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Acute myocardial infarction is the leading cause of cardiovascular-related mortality and chronic heart failure worldwide. As regards treatment, the reperfusion of ischemic tissue generates irreversible damage to the myocardium, which is termed 'cardiac ischemia-reperfusion (IR) injury'. Due to the large number of mitochondria in cardiomyocytes, an increasing number of studies have focused on the roles of mitochondria in IR injury. The primary causes of IR injury are reduced oxidative phosphorylation during hypoxia and the increased production of reactive oxygen species (ROS), together with the insufficient elimination of these oxidative species following reperfusion. IR injury includes the oxidation of DNA, incorrect modifications of proteins, the disruption of the mitochondrial membrane and respiratory chain, the loss of mitochondrial membrane potential (∆Ψm), Ca 2+ over-load, mitochondrial permeability transition pore formation, swelling of the mitochondria, and ultimately, cardiomyocyte necrosis. The present review article discusses the molecular mechanisms of IR injury, and summarizes the metabolic and dynamic changes occurring in the mitochondria in response to IR stress. The mitochondria are strongly recommended as a target for the development of therapeutic agents; however, the appropriate use of agents remains a challenge.

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“…Aside from LDLR, the other members of this family are less well studied specifically for lipoprotein transport at the BBB, and could be a fruitful avenue for future studies to improve CoQ 10 retention by the brain. In addition, the use of LDLR inhibitors may also have potential therapeutic value as a means of increasing cellular CoQ 10 levels in other patient groups which have been associated with a deficiency in the level of this isoprenoid, such as those with cardiovascular disease [ 75 ]. However, further studies will be required before this can be confirmed or refuted.…”

Section: Discussionmentioning

confidence: 99%

CoQ10 Deficient Endothelial Cell Culture Model for the Investigation of CoQ10 Blood–Brain Barrier Transport

Wainwright

Hargreaves

Georgian

et al. 2020

JCM

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Primary coenzyme Q10 (CoQ10) deficiency is unique among mitochondrial respiratory chain disorders in that it is potentially treatable if high-dose CoQ10 supplements are given in the early stages of the disease. While supplements improve peripheral abnormalities, neurological symptoms are only partially or temporarily ameliorated. The reasons for this refractory response to CoQ10 supplementation are unclear, however, a contributory factor may be the poor transfer of CoQ10 across the blood–brain barrier (BBB). The aim of this study was to investigate mechanisms of CoQ10 transport across the BBB, using normal and pathophysiological (CoQ10 deficient) cell culture models. The study identifies lipoprotein-associated CoQ10 transcytosis in both directions across the in vitro BBB. Uptake via SR-B1 (Scavenger Receptor) and RAGE (Receptor for Advanced Glycation Endproducts), is matched by efflux via LDLR (Low Density Lipoprotein Receptor) transporters, resulting in no “net” transport across the BBB. In the CoQ10 deficient model, BBB tight junctions were disrupted and CoQ10 “net” transport to the brain side increased. The addition of anti-oxidants did not improve CoQ10 uptake to the brain side. This study is the first to generate in vitro BBB endothelial cell models of CoQ10 deficiency, and the first to identify lipoprotein-associated uptake and efflux mechanisms regulating CoQ10 distribution across the BBB. The results imply that the uptake of exogenous CoQ10 into the brain might be improved by the administration of LDLR inhibitors, or by interventions to stimulate luminal activity of SR-B1 transporters.

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Clinical Evidence for Q10 Coenzyme Supplementation in Heart Failure: From Energetics to Functional Improvement

Cited by 44 publications

References 93 publications

Plasma Metabolomics Analysis Identifies Abnormal Energy, Lipid, and Amino Acid Metabolism in Abdominal Aortic Aneurysms

Plasma Metabolomics Analysis Identifies Abnormal Energy, Lipid, and Amino Acid Metabolism in Abdominal Aortic Aneurysms

Mitochondria as a therapeutic target for cardiac ischemia‑reperfusion injury (Review)

CoQ10 Deficient Endothelial Cell Culture Model for the Investigation of CoQ10 Blood–Brain Barrier Transport

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