Coenzyme Q10 Prevents Senescence and Dysfunction Caused by Oxidative Stress in Vascular Endothelial Cells
Open accessAbstract
Oxidative damage in endothelial cells is proposed to play an important role in endothelial dysfunction and atherogenesis. We previously reported that the reduced form of coenzyme Q10 (CoQ 10 H 2) effectively inhibits oxidative stress and decelerates senescence in senescence‐accelerated mice. Here, we treated human umbilical vein endothelial cells (HUVECs) with H 2 O 2 and investigated the protective effect of CoQ 10 H 2 against senescence, oxidative damage, and reduction in cellular functions. We found that CoQ 10 H 2 markedly reduced the number of senescence‐associated β‐galactosidase‐positive cells and suppressed the expression of senescence‐associated secretory phenotype‐associated genes in H 2 O 2‐treated HUVECs. Furthermore, CoQ 10 H 2 suppressed the generation of intracellular reactive oxygen species (ROS) but promoted NO production that was accompanied by increased eNOS expression. CoQ 10 H 2 prevented apoptosis and reductions in mitochondrial function and reduced migration and tube formation activity of H 2 O 2‐treated cells. The present study indicated that CoQ 10 H 2 protects endothelial cells against senescence by promoting mitochondrial function and thus could delay vascular aging.
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Treatment with CoQ10H2 of H2O2-induced senescent HUVEC is effective in reducing SA-β gal, SASP release and ROS production, but enhanced NO and eNOS levels.
“For example, a study conducted by Huo et al. has shown that treatment with CoQ10H2 of H2O2-induced senescent human umbilical vein endothelial cells (HUVEC) is effective in reducing SA-β gal, SASP release and ROS production, but enhanced nitric oxide (NO) and endothelial NO synthase (eNOS) levels [67].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [67]
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- Authors
- Huo, J., Xu, Z., Hosoe, K., Kubo, H., Miyahara, H., Dai, J., Mori, M., Sawashita, J., & Higuchi, K.
- Affiliations
- Shinshu University (JP)
- Hebei Medical University (CN)
- Kaneka (Japan) (JP)
- Corresponding author
- Higuchi, Keiichi
- ORCID
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2018-01
- Volume
- 2018
- Issue
- 1
- Pages
- 3181759-3181759
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC6079399
- OpenAlex
- W2812934367
- Cited by
- 87
- References
- 66
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 8 · 2023: 15 · 2022: 14 · 2021: 18 · 2020: 9 · 2019: 12
- FWCI
- 3.47
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (acceptedVersion, other-oa)
- SOAR (Shinshu University) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Kobayashi International Scholarship Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- coenzyme Q10, endothelial cell senescence, oxidative stress, endothelial dysfunction, reactive oxygen species, nitric oxide, endothelial nitric oxide synthase, mitochondrial function, apoptosis, cell migration, tube formation, vascular aging, atherogenesis, human umbilical vein endothelial cells, hydrogen peroxide
- MeSH terms
- Animals, Cells, Cultured, Humans, Ubiquinone, Cellular Senescence, Apoptosis, Oxidative Stress, Endothelial Cells, Mice
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