Targeted Mitochondrial COQ10 Delivery Attenuates Antiretroviral-Drug-Induced Senescence of Neural Progenitor Cells
Open accessAbstract
HIV infection is associated with symptoms of accelerated or accentuated aging that are likely to be driven not only by HIV itself but also by the toxicity of long-term use of antiretroviral drugs. Therefore, it is crucially important to understand the mechanisms by which antiretroviral drugs may contribute to aging. The aim of this study was to investigate the hypothesis that antiretroviral drugs cause increased reactive oxygen species (ROS) generation that results in mitochondrial dysfunction and culminates in promoting cellular senescence. In addition, we applied targeted nanoparticle (NP)-based delivery to specifically enrich mitochondria with coenzyme Q10 (CoQ10) in order to enhance antioxidant protection. The studies employed neural progenitor cells (NPCs), as differentiation of these cells into mature neurons is affected both during HIV infection and in the aging process. Exposure of cultured NPCs to various combinations of HIV antiretroviral therapy (ART) induced a more than 2-fold increase in mitochondrial ROS generation and mitochondrial membrane potential, a more than 50% decrease in oxygen consumption and ATP levels, a 60% decrease in SIRT3 expression, and a 42% decrease in cell proliferation relative to control levels. These alterations were accompanied by a 37% increase in beta-galactosidase staining and a shortening of the telomere length to more than half of the length of controls as assessed by quantitative telomere-FISH labeling, indicating accelerated NPC senescence in response to ART exposure. Importantly, CoQ10 delivered by targeted nanoparticles effectively attenuated these effects. Overall, these results indicate that ART promotes cellular senescence by causing mitochondrial dysfunction, which can be successfully reversed by supplementation with mitochondria-targeted CoQ10.
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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 [65]
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- Authors
- Velichkovska, M., Surnar, B., Nair, M., Dhar, S., & Toborek, M.
- Affiliations
- University of Miami (US)
- Florida International University (US)
- Corresponding author
- Toborek, Michal
- Venue
- Molecular Pharmaceutics
- Publisher
- American Chemical Society (ACS)
- Published
- 2018-12-28
- Volume
- 16
- Issue
- 2
- Pages
- 724-736
- ISSN
- 1543-8384 (ISSN-L)
- 1543-8392
- PMC
- PMC6364271
- OpenAlex
- W2907553798
- Cited by
- 49
- References
- 64
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 4 · 2023: 7 · 2022: 9 · 2021: 8 · 2020: 6 · 2019: 5
- FWCI
- 1.69
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Molecular Pharmaceutics (publishedVersion, other-oa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH072567, MH098891)
- National Institute on Drug Abuse (DA039576, DA040537, DA044579)
- National Heart, Lung, and Blood Institute (HL126559)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- antiretroviral drugs, cellular senescence, neural progenitor cells, coenzyme Q10, mitochondrial dysfunction, reactive oxygen species, targeted nanoparticle delivery, mitochondria-targeted antioxidants, SIRT3, telomere shortening, mitochondrial membrane potential, drug toxicity
- MeSH terms
- Animals, Antioxidants, Cell Line, Mitochondria, Ubiquinone, HIV Infections, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, Anti-Retroviral Agents, Mice, Membrane Potential, Mitochondrial, Nanoparticles, Sirtuin 3, Neural Stem Cells
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