coenzyme-q10 and mitoquinone

Sepsis is one of the main causes of death among critically ill patients. Sepsis pathogenesis includes infection by gram-negative and gram-positive bacteria, fungi, or both; exacerbated inflammatory response; hypotension, with potential to cause vasodilatory shock; and lesser delivery of oxygen to tissues due to impairment of oxygen utilization by cells. The participation of reactive species and/or free radicals such as nitric oxide (NO), peroxynitrite (ONOO

Topics: Adenosine Triphosphate; Animals; Antioxidants; Apoptosis; Humans; Melatonin; Mitochondria; Multiple Organ Failure; Necrosis; NF-kappa B; Organophosphorus Compounds; Oxidative Stress; Selenium; Sepsis; Ubiquinone; Vitamins

The current therapy for patients with stable systolic heart failure is largely limited to treatments that interfere with neurohormonal activation. Critical pathophysiological hallmarks of heart failure are an energetic deficit and oxidative stress, and both may be the result of mitochondrial dysfunction. This dysfunction is not (only) the result of defect within mitochondria per se, but is in particular traced to defects in intermediary metabolism and of the regulatory interplay between excitation-contraction coupling and mitochondrial energetics, where defects of cytosolic calcium and sodium handling in failing hearts may play important roles. In the past years, several therapies targeting mitochondria have emerged with promising results in preclinical models. Here, we discuss the mechanisms and results of these mitochondria-targeted therapies, but also of interventions that were not primarily thought to target mitochondria but may have important impact on mitochondrial biology as well, such as iron and exercise. Future research should be directed at further delineating the details of mitochondrial dysfunction in patients with heart failure to further optimize these treatments.

Topics: Antioxidants; Dietary Supplements; Exercise Therapy; Heart Failure; Humans; Iron; Mitochondria, Heart; Oligopeptides; Organophosphorus Compounds; Trace Elements; Ubiquinone; Vitamins

Neurodegenerative movement disorders mainly include Parkinson's disease (PD), atypical parkinsonisms, Huntington's disease (HD), and Friedreich's ataxia (FA). With mitochondrial dysfunction observed in these diseases, mitochondrial enhancement such as creatine, coenzyme Q10 (CoQ10) and its analogues (idebenone and mitoquinone) has been regarded as a potential treatment.. In this paper, we systematically analysed and summarized the efficacy of mitochondrial enhancement in improving motor and other symptoms in neurodegenerative movement disorders.. We searched the electronic databases PubMed, EMBASE, CINAHL, Cochrane Library and China National Knowledge Infrastructure until September 2013 for eligible randomized controlled trials (RCTs), as well as unpublished and ongoing trials. We calculated the mean differences for continuous data with 95% confidence intervals and pooled the results using a fixed-effect model, if no significant statistical heterogeneity was found (I(2) < 50%).. We included 16 studies with 1,557 randomized patients, which compared creatine, CoQ10 or its analogues with placebo in motor and other symptoms. No significant improvements were found in the motor symptoms of PD, atypical parkinsonisms or HD patients, while only the high dose of idebenone seems to be promising for motor improvement in FA. Certain benefits are found in other symptoms.. There is insufficient evidence to support the use of mitochondrial enhancement in patients with neurodegenerative movement disorders. More well-designed RCTs with large samples are required for further confirmation.

Topics: Animals; Creatine; Dose-Response Relationship, Drug; Humans; Mitochondria; Mitochondrial Diseases; Neurodegenerative Diseases; Organophosphorus Compounds; Randomized Controlled Trials as Topic; Ubiquinone

Multiple studies have determined that obesity increases asthma risk or severity. Metabolic changes of obesity, such as diabetes or insulin resistance, are associated with asthma and poorer lung function. Insulin resistance is also found to increase asthma risk independent of body mass. Conversely, asthma is associated with abnormal glucose and lipid metabolism, insulin resistance, and obesity. Here we review our current understanding of how dietary and lifestyle factors lead to changes in mitochondrial metabolism and cellular bioenergetics, inducing various components of the cardiometabolic syndrome and airway disease.

Topics: Asthma; Bronchial Hyperreactivity; Caloric Restriction; Energy Metabolism; Exercise; Humans; Metabolic Syndrome; Mitochondria; Molecular Targeted Therapy; Obesity; Organophosphorus Compounds; Ubiquinone