Supplementation with the reduced form of Coenzyme Q10 decelerates phenotypic characteristics of senescence and induces a peroxisome proliferator‐activated receptor‐α gene expression signature in SAMP1 mice
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Our present study reveals significant decelerating effects on senescence processes in middle‐aged SAMP1 mice supplemented for 6 or 14 months with the reduced form (Q 10 H 2, 500 mg/kg BW/day) of coenzyme Q 10 (CoQ 10). To unravel molecular mechanisms of these CoQ 10 effects, a genome‐wide transcript profiling in liver, heart, brain and kidney of SAMP1 mice supplemented with the reduced (Q 10 H 2) or oxidized form of CoQ 10 (Q 10) was performed. Liver seems to be the main target tissue of CoQ 10 intervention, followed by kidney, heart and brain. Stringent evaluation of the resulting data revealed that Q 10 H 2 has a stronger impact on gene expression than Q 10, primarily due to differences in the bioavailability. Indeed, Q 10 H 2 supplementation was more effective than Q 10 to increase levels of CoQ 10 in the liver of SAMP1 mice. To identify functional and regulatory connections of the “top 50” (p<0.05) Q 10 H 2‐sensitive transcripts in liver, text mining analysis was used. Hereby, we identified Q 10 H 2‐sensitive genes which are regulated by peroxisome proliferator‐activated receptor‐α and are primarily involved in cholesterol synthesis (e.g. HMGCS1, HMGCL and HMGCR), fat assimilation (FABP5), lipoprotein metabolism (PLTP) and inflammation (STAT‐1). These data may explain, at least in part, the decelerating effects on degenerative processes observed in Q 10 H 2‐supplemented SAMP1 mice.
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The outperformance of CoQ10H2 could be at least in part explained by a higher CoQ10H2 bioavailability at the same concentrations, allowing a more efficient subcellular delivery.
“The reason for this outperformance could be at least in part explained by a higher CoQ10H2 bioavailability at the same concentrations, therefore allowing a more efficient subcellular delivery [66,71].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [71]
CoQ10H2 (ubiquinol) is even more efficient than CoQ10 itself in reverting senescence markers expression, both in vitro and in vivo.
“CoQ10H2 (or ubiquinol), the reduced form of CoQ10, is even more efficient than CoQ10 itself in reverting senescence markers expression, both in vitro and in vivo [66,71].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [71]
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Schmelzer, C., Kitano, M., Hosoe, K., & ring, F. D. O. (2011) · Journal of Clinical Biochemistry and Nutrition · doi:10.3164/jcbn.11-19 · Cited by 19 · see citing works
Self-citationFakhrolmobasheri, M., Hosseini, M. S., Shahrokh, S. G., Mohammadi, Z. S., Kahlani, M.-J., Majidi, S.-E., & Zeinalian, M. (2021) · Advanced Pharmaceutical Bulletin · doi:10.34172/apb.2023.026 · Cited by 17 · see citing works
Fischer, A., Onur, S., Schmelzer, C., & Döring, F. (2012) · BMC Research Notes · doi:10.1186/1756-0500-5-540 · Cited by 15 · see citing works
Self-citationShamardl, H. A., Elashmony, S. M., Kamel, H. F. M., & Fatani, S. H. (2017) · The American Journal of the Medical Sciences · doi:10.1016/j.amjms.2017.04.007 · Cited by 13 · see citing works
Daei, S., Ildarabadi, A., Goodarzi, S., & Mohammadi‐Sartang, M. (2024) · High Blood Pressure & Cardiovascular Prevention · doi:10.1007/s40292-024-00630-8 · Cited by 12 · see citing works
Micronutrient Metabolism in Hemodialysis Patients
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Targeting Mitochondrial Defects to Increase Longevity in Animal Models of Neurodegenerative Diseases
Casajús-Pelegay, E., Puzzo, F., Yılmazer, A., & Cagin, U. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-12668-1_5 · Cited by 12 · see citing works
Ubiquinol Reduces Muscle Wasting but Not Fatigue in Tumor-Bearing Mice
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Determination of the coenzyme Q 10 status in a large C aucasian study population
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Facing challenges in an ageing world
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Self-citationImportance of CoQ10-dependent Redox Activity in Aging
López‐Lluch, G. (2021) · Healthy ageing and longevity · doi:10.1007/978-3-030-84965-8_9 · Cited by 2 · see citing works
Hirose, K., Chang, S., Yu, H., Wang, J., Barca, E., Chen, X. L., Khyeam, S., Tajima, K., Yoneshiro, T., Kajimura, S., et al. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/755793 · Cited by 2 · see citing works
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Fenofibrate: Panacea for Aging-Related Conditions?
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Self-citationAn in vivo system for the identification of ligands for peroxisome proliferatoractivated receptors
Lee, R. H. (2015) · TSpace (University of Toronto)
Igarashi, Y., Hamada, S., Dai, J. M., Mori, M., Miyahara, H., Sawashita, J., & Higuchi, K. (2025) · Experimental Gerontology · doi:10.1016/j.exger.2025.112924
Self-citationCoQ10 Supplementation for Healthy Longevity
López‐Lluch, G. (2026) · Healthy ageing and longevity · doi:10.1007/978-3-032-11608-6_6
- Authors
- Schmelzer, C., Kubo, H., Mori, M., Sawashita, J., Kitano, M., Hosoe, K., Boomgaarden, I., Döring, F., & Higuchi, K.
- Affiliations
- Christian-Albrechts-Universität zu Kiel (DE)
- Kaneka (Japan) (JP)
- Shinshu University (JP)
- Corresponding author
- Döring, Frank
- Venue
- Molecular Nutrition & Food Research
- Publisher
- Wiley
- Published
- 2010-06
- Volume
- 54
- Issue
- 6
- Pages
- 805-815
- ISSN
- 1613-4125 (ISSN-L)
- 1613-4133
- OpenAlex
- W1995774391
- Cited by
- 53
- References
- 56
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 5 · 2019: 7 · 2018: 2 · 2017: 3 · 2016: 1 · 2015: 6 · 2014: 5 · 2013: 3 · 2012: 2
- FWCI
- 1.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Nutrition & Food Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (21650097)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- coenzyme Q10, aging, senescence, SAMP1 mice, PPARα, gene expression signatures, liver, cholesterol biosynthesis, lipoprotein metabolism, inflammation, bioavailability, dietary supplementation
- MeSH terms
- Aging, Animals, Eating, Female, Gene Expression Regulation, Liver, Oxidation-Reduction, Phenotype, Ubiquinone, Dietary Supplements, Gene Expression Profiling, PPAR alpha, Mice
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