Coenzyme Q10 is an essential cofactor in the electron transport chain and serves as an important antioxidant in both mitochondria and lipid membranes. CoQ10 is also an obligatory cofactor for the function of uncoupling proteins. Furthermore, dietary supplementation affecting CoQ10 levels has been shown in a number of organisms to cause multiple phenotypic effects. However, the molecular mechanisms to explain pleiotrophic effects of CoQ10 are not clear yet and it is likely that CoQ10 targets the expression of multiple genes. We therefore utilized gene expression profiling based on human oligonucleotide sequences to examine the expression in the human intestinal cell line CaCo-2 in relation to CoQ10 treatment. CoQ10 caused an increased expression of 694 genes at threshold-factor of 2.0 or more. Only one gene was down-regulated 1.5-2-fold. Real-time RT-PCR confirmed the differential expression for seven selected target genes. The identified genes encode proteins involved in cell signalling (n = 79), intermediary metabolism (n = 58), transport (n = 47), transcription control (n = 32), disease mutation (n = 24), phosphorylation (n = 19), embryonal development (n = 13) and binding (n = 9). In conclusion, these findings indicate a prominent role of CoQ10 as a potent gene regulator. The presently identified comprehensive list of genes regulated by CoQ10 may be used for further studies to identify the molecular mechanism of CoQ10 on gene expression.
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http://dx.doi.org/10.1016/j.biocel.2004.11.017 | DOI Listing |
Clin J Am Soc Nephrol
January 2025
Department of Medicine, Division of Nephrology, University of California, Davis, CA, USA.
Background: Mitochondria-driven oxidative/redox stress and inflammation play a major role in chronic kidney disease (CKD) pathophysiology. Compounds targeting mitochondrial metabolism may improve mitochondrial function, inflammation, and redox stress; however, there is limited evidence of their efficacy in CKD.
Methods: We conducted a pilot randomized, double-blind, placebo-controlled crossover trial comparing the effects of 1200 mg/day of coenzyme Q10 (CoQ10) or 1000 mg/day of nicotinamide riboside (NR) supplementation to placebo in 25 people with moderate-to-severe CKD (estimated glomerular filtration rate [eGFR] <60mL/min/1.
Int J Biol Macromol
January 2025
State Key Laboratory of Food Science and Resources, School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu 214122, China.
Int J Syst Evol Microbiol
January 2025
Guangdong Provincial Key Laboratory of Marine Biology, Shantou University, Shantou 515063, PR China.
Marine biofilms were newly revealed as a bank of hidden microbial diversity and functional potential. In this study, a Gram-stain-negative, aerobic, oval and non-motile bacterium, designated LMIT008, was isolated from the biofilm of concrete breakwater structures located in the coastal area of Shantou, PR China. Strain LMIT008 was found to grow at salinities of 1-7% NaCl, at pH 5-8 and at temperatures 10-40 °C.
View Article and Find Full Text PDFInflammation
January 2025
Department of Chemistry, University of Agriculture Faisalabad, Faisalabad, Pakistan.
Parkinson's disease (PD) stands as the sec most prevalent incapacitating neurodegenerative disorder characterized by deterioration of dopamine-producing neurons in the substantia nigra. Coenzyme Q10 (CoQ10) has garnered attention as a potential antioxidant, anti-inflammatory agent and enhancer of mitochondrial complex-I activity. This study aimed to examine and compare the effectiveness of liposomal and non-encapsulated CoQ10 in rotenone induced-PD mouse model over a 21-day treatment duration.
View Article and Find Full Text PDFJ Adv Res
January 2025
Department of Oncology, The First Affiliated Hospital, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences Xi'an Jiaotong University Xi'an Shanxi China. Electronic address:
Introduction: Ferroptosis is an iron-dependent form of cell death triggered by the excessive accumulation of lipid peroxides. Understanding the regulatory mechanisms of ferroptosis and developing strategies to target this process hold significant clinical applications in tumor therapy.
Objective: Our study aims to search for novel candidate genes involved in the regulation of ferroptosis and to investigate their mechanism of action in ferroptosis and tumor therapy.
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