Inhibition of Stress Induced Premature Senescence in Presenilin-1 Mutated Cells with Water Soluble Coenzyme Q10
Open accessAbstract
A water-soluble formulation of CoQ10 (WS-CoQ10) was shown to stabilize mitochondria and prevent oxidative stress-induced neuronal death. Presenilin-1 (PS-1)-mutated Alzheimer's Disease (AD) fibroblasts (PSAF) were used for studying the effects of PS-1 mutation. PS-1 mutation correlated to increased reactive oxygen species (ROS) production and stress induced premature senescence (SIPS) in PSAF; WS-CoQ10 treatment decreased ROS generation, increased population doublings, and postponed SIPS. Treated PSAF had higher PCNA expression, and lower levels of MnSOD, p21, p16Ink4A, and Rb. WS-CoQ10 caused the resumption of autophagy in PSAF. Thus, WS-CoQ10 as inhibitor of SIPS and ameliorator of autophagy could be an effective prophylactic/therapeutic agent for AD.
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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 [60]
Similar beneficial effects of CoQ10 have been obtained in cancer and Alzheimer's disease, in whose pathogenesis OS plays a predominant role.
“Similar beneficial effects have been obtained in cancer and Alzheimer’s disease (AD), in whose pathogenesis OS plays a predominant role [60,61].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [60]
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References 42 · Cited by 39
- Authors
- Ma, D., Stokes, K., Mahngar, K., Domazet-Damjanov, D., Sikorska, M., & Pandey, S.
- Affiliations
- University of Windsor (CA)
- Institute for Biological Sciences (CA)
- Corresponding author
- Pandey, Siyaram
- Venue
- Mitochondrion
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 17
- Pages
- 106-115
- ISSN
- 1567-7249 (ISSN-L)
- OpenAlex
- W2078163450
- Cited by
- 39
- References
- 42
- Citations by year
- 2026: 5 · 2025: 3 · 2023: 4 · 2022: 5 · 2021: 3 · 2020: 4 · 2019: 5 · 2018: 1 · 2017: 3 · 2016: 3 · 2015: 3
- FWCI
- 1.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Mitochondrion (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- Natural Sciences and Engineering Research Council of Canada (238744-2009)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- stress-induced premature senescence, presenilin 1 mutations, Alzheimer's disease, reactive oxygen species, oxidative stress, autophagy, fibroblasts, p16INK4a, p21, manganese superoxide dismutase, PCNA, neuroprotection
- MeSH terms
- Aging, Alzheimer Disease, Cells, Cultured, Female, Fibroblasts, Humans, Male, Stress, Physiological, Ubiquinone, Vitamins, Presenilin-1
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