The mitochondria are the powerhouses of the cell, producing ATP, a kind of universal energy used in cellular functions. Mitochondrial dysfunction is an important part of the aging process. As cells age, the effectiveness of the respiratory chain diminishes, increasing electron leakage and reducing ATP generation [1].

As mitochondria become more dysfunctional with age, there is an increased production of reactive oxygen species (ROS), causing further mitochondrial deterioration and cellular damage. Strikes from reactive oxygen species can delete sections of mitochondrial DNA and cause damage to important components of the cell. This is thought to be a primary reason we age and is part of the aging hallmark of genomic instability [2-3].

There are other ways that mitochondria can contribute to the aging process; for example, mitochondrial dysfunction may affect apoptotic signaling by increasing the likelihood that the mitochondria permeabilize in response to stress, triggering inflammatory reactions via ROS-mediated and/or permeabilization-facilitated mechanisms [4-5].

Another way is that mitochondrial dysfunction might also affect cellular signaling and communication between organelles by affecting the interface between the outer mitochondrial membrane and the endoplasmic reticulum [6].

To that end, we wanted to highlight a recently published open access paper that discusses the idea of targeting mitochondria in order to counteract age-related cellular dysfunction [7].


Senescence is related to the loss of cellular homeostasis and functions, which leads to a progressive decline in physiological ability and to aging-associated diseases. Since mitochondria are essential to energy supply, cell differentiation, cell cycle control, intracellular signaling and Ca2+ sequestration, fine-tuning mitochondrial activity appropriately, is a tightrope walk during aging. For instance, the mitochondrial oxidative phosphorylation (OXPHOS) ensures a supply of adenosine triphosphate (ATP), but is also the main source of potentially harmful levels of reactive oxygen species (ROS). Moreover, mitochondrial function is strongly linked to mitochondrial Ca2+ homeostasis and mitochondrial shape, which undergo various alterations during aging. Since mitochondria play such a critical role in an organism’s process of aging, they also offer promising targets for manipulation of senescent cellular functions. Accordingly, interventions delaying the onset of age-associated disorders involve the manipulation of mitochondrial function, including caloric restriction (CR) or exercise, as well as drugs, such as metformin, aspirin, and polyphenols. In this review, we discuss mitochondria’s role in and impact on cellular aging and their potential to serve as a target for therapeutic interventions against age-related cellular dysfunction.


There are many other mechanisms by which dysfunctional mitochondria are potentially influencing the aging processes. The best way to find out how much influence they have is to test it by repairing the damage, restoring mitochondrial function, and observing what happens.


[1] Green, D. R., Galluzzi, L., & Kroemer, G. (2011). Mitochondria and the autophagy–inflammation–cell death axis in organismal aging. Science, 333(6046), 1109-1112.

[2] Edgar, D., Shabalina, I., Camara, Y., Wredenberg, A., Calvaruso, M. A., Nijtmans, L., … & Trifunovic, A. (2009). Random point mutations with major effects on protein-coding genes are the driving force behind premature aging in mtDNA mutator mice. Cell metabolism, 10(2), 131-138.

[3] Hiona, A., Sanz, A., Kujoth, G. C., Pamplona, R., Seo, A. Y., Hofer, T., … & Servais, S. (2010). Mitochondrial DNA mutations induce mitochondrial dysfunction, apoptosis and sarcopenia in skeletal muscle of mitochondrial DNA mutator mice. PloS one, 5(7), e11468.

[4] Kroemer, G., Galluzzi, L., & Brenner, C. (2007). Mitochondrial membrane permeabilization in cell death. Physiological reviews, 87(1), 99-163.

[5] Green, D. R., Galluzzi, L., & Kroemer, G. (2011). Mitochondria and the autophagy–inflammation–cell death axis in organismal aging. Science, 333(6046), 1109-1112.

[6] Raffaello, A., & Rizzuto, R. (2011). Mitochondrial longevity pathways. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1813(1), 260-268.

[7] Madreiter-Sokolowski, C. T., Sokolowski, A. A., Waldeck-Weiermair, M., Malli, R., & Graier, W. F. (2018). Targeting Mitochondria to Counteract Age-Related Cellular Dysfunction. Genes, 9(3), 165.

About the author

Steve Hill

Steve serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic as well as attending various medical industry conferences. In 2019 he was listed in the top 100 journalists covering biomedicine and longevity research in the industry report – Top-100 Journalists covering advanced biomedicine and longevity created by the Aging Analytics Agency. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, and, Keep me Prime, and New Economy Magazine. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project. In 2015 he led the Major Mouse Testing Program (MMTP) for the International Longevity Alliance and in 2016 helped the team of the SENS Research Foundation to reach their goal for the OncoSENS campaign for cancer research.
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