Cited by 265Coenzyme Q10 studies and effectsInflammatory mediators and NSAID effectsNF-κB Signaling Pathways

Functions of coenzyme Q10 in inflammation and gene expression

Schmelzer, Constance, Lindner, Inka, Rimbach, Gerald, Niklowitz, Petra, Menke, Thomas, Döring, Frank·2008·BioFactors

Abstract

Clinical studies demonstrated the efficacy of Coenzyme Q 10 (CoQ 10) as an adjuvant therapeutic in cardiovascular diseases, mitochondrial myopathies and neurodegenerative diseases. More recently, expression profiling revealed that Coenzyme Q 10 (CoQ 10) influences the expression of several hundred genes. To unravel the functional connections of these genes, we performed a text mining approach using the Genomatix BiblioSphere. We identified signalling pathways of G‐protein coupled receptors, JAK/STAT, and Integrin which contain a number of CoQ 10 sensitive genes. Further analysis suggested that IL5, thrombin, vitronectin, vitronectin receptor, and C‐reactive protein are regulated by CoQ 10 via the transcription factor NFκB1. To test this hypothesis, we studied the effect of CoQ 10 on the NFκB1‐dependent pro‐inflammatory cytokine TNF‐α. As a model, we utilized the murine macrophage cell lines RAW264.7 transfected with human apolipoprotein E3 (apoE3, control) or pro‐inflammatory apoE4. In the presence of 2.5 μM or 75 μM CoQ 10 the LPS‐induced TNF‐α response was significantly reduced to 73.3±2.8% and 74.7±8.9% in apoE3 or apoE4 cells, respectively. Therefore, the in silico analysis as well as the cell culture experiments suggested that CoQ 10 exerts anti‐inflammatory properties via NFκB1‐dependent gene expression.

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Crossref · 10.1002/biof.5520320121

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  • Coenzyme Q10 has anti-inflammatory effects via the suppression of the activation of NF-kB and through the modulation of the transcription of genes governing pro-inflammatory JAK/STAT pathways.

    “CoQ10 also has anti-inflammatory effects via the suppression of the activation of NF-κB and through the modulation of the transcription of genes governing pro-inflammatory JAK/STAT pathways [178].”

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Authors
Schmelzer, C., Lindner, I., Rimbach, G., Niklowitz, P., Menke, T., & Döring, F.
Affiliations
  • Christian-Albrechts-Universität zu Kiel (DE)
  • Witten/Herdecke University (DE)
Corresponding author
Döring, Frank
Venue
BioFactors
Publisher
Wiley
Published
2008-01
Volume
32
Issue
1-4
Pages
179-183
ISSN
  • 0951-6433 (ISSN-L)
  • 1872-8081
OpenAlex
W2014824398
Cited by
265
References
17
Citations by year
2026: 13 · 2025: 13 · 2024: 11 · 2023: 19 · 2022: 27 · 2021: 33 · 2020: 16 · 2019: 14 · 2018: 13 · 2017: 13 · 2016: 12 · 2015: 15 · 2014: 11 · 2013: 13 · 2012: 15
FWCI
3.70
Type
journal article
Language
en
Open access
closed
Locations
  • BioFactors (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
coenzyme Q10, inflammation, gene expression, NFKB1, TNF-α, anti-inflammatory activity, APOE ε4, APOE3, macrophages, lipopolysaccharide, G protein-coupled receptors, JAK/STAT signaling, integrin signaling, C-reactive protein, vitronectin, IL-5, thrombin
MeSH terms
Animals, Cell Line, Computer Simulation, Inflammation, Lipopolysaccharides, Macrophages, Models, Biological, Tumor Necrosis Factor-alpha, Ubiquinone, Signal Transduction, Gene Expression, Mice

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