The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Moderation of mitochondrial respiration mitigates metabolic syndrome of aging
Abstract
Significance: The efforts toward minimizing oxidative stress and maintaining mitochondrial energy metabolism for promoted healthy aging are at the forefront of current research on aging. We have characterized a treatment that, by reversible inhibition of mitochondrial respiration in mice through cytochrome c oxidase (CcO), markedly improves mitochondrial bioenergetics and delays the lead health concerns associated with aging in mice. We demonstrated that chronic moderate inhibition of CcO reduces ATP synthesis, promotes mitochondrial biogenesis and mitophagy, subsequently decreases ROS production and mitochondrial decay, and rectifies vital cellular energy metabolism regulators, thus, effectively refining energy homeostasis and curbing obesity and glucose irregularities linked to aging.
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“Mild inhibition of mitochondrial ATP synthesis with TPPthiazole can improve metabolic health in aging mice, reducing visceral fat and improving glucose tolerance, mitochondrial quality and oxidative metabolism 166 .”
From Hallmarks of aging: An expanding universe (2023) · cites this paper as [166]
In the citing paper
“| Mitochondrial dysfunction | Mouse | TPP-thiazole (inhibitor of respiratory chain complex IV) | Improved mitochondrial metabolism, reduced visceral fat and higher glucose tolerance in old mice | 166 |”
From Hallmarks of aging: An expanding universe (2023) · cites this paper as [166]
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mTOR is a key modulator of ageing and age-related disease
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The role of mitochondria in aging
Bratic, A., & Larsson, N.-G. (2013) · Journal of Clinical Investigation · doi:10.1172/jci64125 · Cited by 1,087
Overexpression of Atg5 in mice activates autophagy and extends lifespan
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López-Lluch, G. (2017) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2016.12.005 · Cited by 103 · cited 1×
“The CcO activity of the 14-mo-old untreated control group was ≃ 47% lower than that of the 2-mo-old untreated control, consistent with the concept that mitochondria deteriorate through aging (16).”
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Cited by
Sorted by citations
Hallmarks of aging: An expanding universe
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2023) · Cell · doi:10.1016/j.cell.2022.11.001 · Cited by 6,549
Mitochondrial and metabolic dysfunction in ageing and age-related diseases
Amorim, J. A., Coppotelli, G., Rolo, A. P., Palmeira, C. M., Ross, J. M., & Sinclair, D. A. (2022) · Nature Reviews Endocrinology · doi:10.1038/s41574-021-00626-7 · Cited by 990
Pini, M., Czibik, G., Sawaki, D., Mezdari, Z., Braud, L., Delmont, T., Mercedes, R., Martel, C., Buron, N., Marcelin, G., et al. (2021) · Aging Cell · doi:10.1111/acel.13421 · Cited by 43
Metadata
- Authors
- Tavallaie, M., Voshtani, R., Deng, X., Qiao, Y., Jiang, F., Collman, J. P., & Fu, L.
- Affiliations
- Shanghai Key Laboratory for Molecular Engineering of Chiral Drugs, School of Pharmacy, Shanghai Jiao Tong University, 200240 Shanghai, China;
- Department of Genetics and Immunology, School of Life Sciences, Shanghai Jiao Tong University, 200240 Shanghai, China;
- Department of Chemistry, Stanford University, Stanford, CA 94305
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2020-04-17
- Volume
- 117
- Issue
- 18
- Pages
- 9840-9850
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 71
- References
- 9
- Language
- en
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