ObjectiveTo systematically review the efficacy of coenzyme Q10 as adjuvant therapy for patients with heart failure. MethodsDatabases including PubMed, The Cochrane Library (Issue 7, 2015), EMbase, CBM, CNKI, WanFang Data and VIP were searched to collect randomized controlled trials (RCTs) about coenzyme Q10 in the treatment of heart failure from inception to June 2015. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then, meta-analysis was performed using RevMan 5.3 software. ResultsA total of 24 RCTs involving 2883 patients were included. The results of meta-analysis showed that:compared with the control group, the coenzyme Q10 group had the lower mortality (RR=0.62, 95%CI 0.47 to 0.83, P=0.001), higher eject fraction (EF) level (MD=3.81, 95%CI 1.22 to 6.40, P=0.004), lower NYHA cardiac function classification (MD=-0.31, 95%CI -0.35 to -0.26), P<0.00001), and higher exercise tolerance (SMD=0.70, 95%CI 0.31 to 1.09, P=0.0005). ConclusionCurrent evidence shows that, coenzyme Q10 can reduce mortality, NYHA cardiac function classification and improve EF and exercise tolerance in patients with heart failure. Due to the limited quality of included studies, the above conclusion still needs to be verified by more high quality studies.
ObjectiveTo systematically review the efficacy and safety of CoQ10 for idiopathic oligoasthenoteratozoospermia (iOAT). MethodsWe searched databases including PubMed, EMbase, MEDLINE, The Cochrane Library, CBM, CNKI, VIP and WanFang Data from inception to May 31th 2016 for randomized controlled trials (RCTs) on CoQ10 in the treatment of iOAT. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then, meta-analysis was performed using RevMan 5.3 software. ResultsSeven RCTs involving 803 patients were included. The results of meta-analysis showed, compared with the control group, the CoQ10 group could significantly increase sperm concentration (MD=3.37, 95%CI 0.68 to 6.05, P=0.01), the number of A grade spermatozoa (MD=5.06, 95%CI 3.84 to 6.28, P < 0.000 01), the number of A+B grade spermatozoa (MD=7.72, 95%CI 4.19 to 11.26, P < 0.000 1), the rate of morphologically normal sperm (MD=1.89, 95%CI 0.63 to 3.16, P=0.003) and sperm coenzyme Q10 level (MD=40.02, 95%CI 24.73 to 55.31, P < 0.000 01), while not improve the levels of serum sex hormone (FSH: MD=–3.48, 95%CI –5.17 to –1.79, P < 0.000 1; LH: MD=–3.23, 95%CI –7.55 to 1.08, P=0.14; T: MD=0.45, 95%CI –3.31 to 4.20, P=0.82). No significant difference in adverse event was noted between two groups. ConclusionThe evidence suggests that CoQ10 as empiric medical therapy for iOAT with low non-serious adverse event associated, may improve sperm concentration and percent sperm motility. However, the strength of evidence is low due to high risk of bias of the included studies. More rigorous studies are needed to verify the above conclusion.
Epilepsy is a complex disease spectrum, because of long-term recurrent seizures and seriously affect the quality of life of patients, it is of great significance to explore the pathogenesis of epilepsy and actively seek new therapeutic targets. In this paper, the pathogenesis of epilepsy related to mitochondrial pathway was discussed from the aspects of energy depletion, oxidative stress damage, impaired calcium homeostasis, increased glutamic acid release, mitochondrial DNA mutation, Coenzyme Q10 deficiency, abnormal mitochondrial movement and change, and relevant therapeutic ideas were proposed. This paper shows that mitochondrial function affects the onset of epilepsy from various ways. Further understanding of the relationship between mitochondria and the onset of epilepsy is beneficial to find new therapeutic targets and develop new therapies beyond the control of epilepsy.