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Mitochondria and Their Role in Aging

Mitochondria are organelles responsible for energy production, and their dysfunction is linked to aging. Research is focusing on identifying mechanisms that contribute to mitochondrial dysfunction, and exploring ways to target them therapeutically.

Mitochondria are organelles within the cells of all eukaryotes, and they play a vital role in energy production. Mitochondrial dysfunction is increasingly being linked to aging, as mitochondrial damage accumulates over time, leading to age-associated declines in cellular function and health. In recent years, research has focused on identifying mechanisms that contribute to mitochondrial dysfunction and exploring ways to target them therapeutically (Johnson et al., 2021)

The main purpose of mitochondria is to generate energy in the form of Adenosine triphosphate (ATP), which is necessary for many cellular functions. Mitochondria are especially important for highly active cells, such as muscle and brain cells, which require large amounts of energy to perform their functions. During the process of producing ATP, reactive oxygen species (ROS) are also produced, which can cause oxidative damage to the cell. As cells age, ROS levels increase and mitochondrial activity decreases, resulting in impaired energy production (Stefanatos & Sanz, 2018)). 

In addition to oxidative damage, other factors contribute to mitochondrial dysfunction with aging. For example, genetic mutations in mitochondrial DNA accumulate over time, leading to decreases in protein synthesis and energy production (Yan et al., 2019). Mitochondrial structure is also affected by aging, with a decrease in the number and size of cristae, the inner membrane folds involved in energy production (Miwa et al., 2022). These changes can lead to a decrease in the efficiency of ATP production, further contributing to mitochondrial dysfunction.

It is becoming increasingly clear that mitochondrial dysfunction plays an important role in aging, and research is now focusing on how to target this pathway therapeutically. One approach is to use drugs that target the enzymes involved in energy production and ROS production, in order to restore mitochondrial function. This approach is called “mitochondrial targeted therapy.” Some ingredients in NOVOS Core serve this purpose. The goal is to protect the mitochondria from damage and improve energy production, thereby reducing the production of reactive oxygen species (ROS) that can contribute to cellular damage and disease (Hirano et al., 2018). 

Another approach is to use compounds that target specific pathways involved in mitochondrial aging, such as the sirtuin pathway (Zhang et al., 2020). Other ingredients in NOVOS Core activate multiple sirtuin pathways. 

Finally, increasing evidence suggests that caloric restriction or intermittent fasting may help to slow the rate of mitochondrial aging by reducing oxidative stress and maintaining mitochondrial integrity (Zhao et al., 2022). 

Overall, mitochondrial dysfunction is an important factor in aging, and research into therapeutic approaches is ongoing. Understanding the mechanisms that drive mitochondrial aging, and developing strategies to target these pathways, will be essential for developing therapies that can delay or prevent age-related diseases.



  1. Hirano, M., Emmanuele, V., & Quinzii, C. M. (2018). Emerging therapies for mitochondrial diseases. Essays in biochemistry, 62(3), 467–481. https://doi.org/10.1042/EBC20170114
  2. Johnson, J., Mercado-Ayon, E., Mercado-Ayon, Y., Dong, Y. N., Halawani, S., Ngaba, L., & Lynch, D. R. (2021). Mitochondrial dysfunction in the development and progression of neurodegenerative diseases. Archives of biochemistry and biophysics, 702, 108698. https://doi.org/10.1016/j.abb.2020.108698
  3. Miwa, S., Kashyap, S., Chini, E., & von Zglinicki, T. (2022). Mitochondrial dysfunction in cell senescence and aging. The Journal of clinical investigation, 132(13), e158447. https://doi.org/10.1172/JCI158447
  4. Stefanatos, R., & Sanz, A. (2018). The role of mitochondrial ROS in the aging brain. FEBS letters, 592(5), 743–758. https://doi.org/10.1002/1873-3468.12902
  5. Yan, C., Duanmu, X., Zeng, L., Liu, B., & Song, Z. (2019). Mitochondrial DNA: Distribution, Mutations, and Elimination. Cells, 8(4), 379. https://doi.org/10.3390/cells8040379
  6. Zhang, J., Xiang, H., Liu, J., Chen, Y., He, R. R., & Liu, B. (2020). Mitochondrial Sirtuin 3: New emerging biological function and therapeutic target. Theranostics, 10(18), 8315–8342. https://doi.org/10.7150/thno.45922
  7. Zhao, Y., Jia, M., Chen, W., & Liu, Z. (2022). The neuroprotective effects of intermittent fasting on brain aging and neurodegenerative diseases via regulating mitochondrial function. Free radical biology & medicine, 182, 206–218. https://doi.org/10.1016/j.freeradbiomed.2022.02.021


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