Anti-ageing effects of ubiquinone and ubiquinol in a senescence model of human dermal fibroblasts
Abstract
Coenzyme Q 10 (CoQ 10) is an endogenous lipophilic quinone found in equilibrium between its oxidised (ubiquinone) and reduced (ubiquinol) form, ubiquitous in biological membranes and endowed with antioxidant and bioenergetic properties, both crucial to the ageing process. CoQ 10 biosynthesis decreases with age in different tissues including skin and its biosynthesis can be modulated by 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors such as statins. Statin-induced CoQ 10 deprivation has previously been shown to be associated with the development of a senescence phenotype in cultured human dermal fibroblasts (HDF), hence this model was used to further investigate the role of CoQ 10 in skin ageing. The present study aimed to compare the bioavailability of exogenously added CoQ 10, in the form of ubiquinone or ubiquinol, to CoQ 10-deprived HDF, and to determine their efficacy in rescuing the senescent phenotype induced by CoQ 10 deprivation. First, additional senescence markers were implemented to further support the pro-ageing effect of statin-induced CoQ 10 deprivation in HDF. Indeed, numerous senescence-associated secretory phenotype (SASP) markers such as p21, IL-8, CXCL1, and MMP-1 were upregulated, whereas components of the extracellular matrix were downregulated (elastin, collagen type 1). Next, we showed that CoQ 10 supplementation to statin-treated HDF was able to counteract CoQ 10 deprivation and rescued the development of selected senescence/ageing markers in HDF. Ubiquinol resulted more bioavailable than ubiquinone at the same concentration (15 μg/mL) and it significantly improved the cellular oxidative status even within isolated mitochondria highlighting an effective subcellular delivery. Ubiquinol was also more efficient compared to ubiquinone in reverting the expression of the senescent phenotype, quantified in terms of β-galactosidase positivity, p21, collagen type 1, and elastin at the gene and protein expression levels. In conclusion, our results highlight the pivotal role of CoQ 10 for skin vitality and strongly support the use of both forms as a beneficial and effective anti-ageing skin care treatment.
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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 [66]
CoQ10 deficiency has been linked to increased p21 expression, enhanced SASP production and downregulation of collagen type I and elastin.
“Regarding senescence, CoQ10 deficiency has also been linked to increased p21 expression (a regulator of cell cycle progression), enhanced SASP production and downregulation of some extracellular matrix components (collagen type I and elastin) [66].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [66]
Coenzyme Q10, SkQ1, mitoquinone and methylene blue are among mitochondria targeted antioxidants exerting a role in counteracting OS-induced senescence, with CoQ10 being the most studied.
“Coenzyme Q10 (CoQ10), SkQ1 (a.k.a. visomitin), mitoquinone (MitoQ) and methylene blue are among the mitochondria targeted antioxidants exerting a role in counteracting OS-induced senescence, with CoQ10 being the most studied (Table 1 and Table 2) [57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [66]
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 [66]
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- Authors
- Marcheggiani, F., Kordes, S., Cirilli, I., Orlando, P., Silvestri, S., Vogelsang, A., Möller, N., Blatt, T., Weise, J. M., Damiani, E., & Tiano, L.
- Affiliations
- Marche Polytechnic University (IT)
- Beiersdorf (Germany) (DE)
- Università di Camerino (IT)
- Corresponding author
- Tiano, Luca
- ORCID
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2021-03
- Volume
- 165
- Pages
- 282-288
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W3124649072
- Cited by
- 48
- References
- 56
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 12 · 2023: 9 · 2022: 9 · 2021: 5
- FWCI
- 2.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- coenzyme Q10, ubiquinol, skin aging, human dermal fibroblasts, cellular senescence, statins, senescence-associated secretory phenotype, oxidative stress, collagen type 1, elastin
- MeSH terms
- Aging, Antioxidants, Fibroblasts, Humans, Ubiquinone
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