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Decline of Mitophagy Appears to Accelerate Heart Aging

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As aging is a major risk factor for developing cardiovascular diseases, their prevalence rises rapidly with advancing age. A new study sheds light on our cells’ declining ability to provide quality control for mitochondria, which spurs other aspects of aging.

The loss of mitophagy accelerates aging

The mitochondria are well-known as being the powerhouses of the cell, as they convert the nutrients we consume into adenosine triphosphate (ATP), a universal form of cellular energy that fuels the many functions our cells need to perform. As we grow older, our mitochondria begin to become increasingly damaged and dysfunctional, and with that comes a decline of function and energy production.

One possible reason mitochondrial function starts to falter as we age is due to the failure of autophagy, a cellular quality control system, and one of its sub-processes, mitophagy. Essentially, autophagy is our cells’ way of removing damaged components, allowing them to be replaced with healthy ones. Mitophagy occurs when autophagy selectively breaks down worn out or damaged mitochondria.

Mitophagy occurs through the cells in our body and is essential for keeping us healthy. In tissues with high energy requirements, including the heart, the decline of mitophagy is almost certainly a key factor in the development of age-related diseases.

Mitochondrial dysfunction is one of the hallmarks of aging, and this new review offers a good summary of the current knowledge of autophagy and mitophagy in the context of aging [1]. The researchers discuss how changes to these important maintenance processes contribute to aging of the heart and the onset of age-related cardiovascular diseases.

Aging is associated with structural and functional changes in the heart and is a major risk factor in developing cardiovascular disease. Many recent studies have focused on increasing our understanding of the basis of aging at the cellular and molecular levels in various tissues, including the heart. It is known that there is an age-related decline in cellular quality control pathways such as autophagy and mitophagy, which leads to accumulation of potentially harmful cellular components in cardiac myocytes. There is evidence that diminished autophagy and mitophagy accelerate the aging process, while enhancement preserves cardiac homeostasis and extends life span. Here, we review the current knowledge of autophagy and mitophagy in aging and discuss how age-associated alterations in these processes contribute to cardiac aging and age-related cardiovascular diseases.

How can we fix it?

There are a number of possible approaches we might use to address the age-related decline of mitophagy, and the research community is currently exploring them.



The seemingly most popular approach right now is to attempt to increase the energy output of mitochondria and somewhat correct their dysfunction by delivering nicotinamide adenine dinucleotide (NAD+) precursors to the cells. Of the currently spotlighted precursors, nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) and the most popular; however, niacin is an older and more studied precursor. NR and NMN are both in human trials to see if they might be useful in mitigating age-related decline. We have covered the topic of NAD+ and its relationship to aging extensively, and you can learn more about it here.

Another approach currently being explored is the delivery of mitochondrially targeted antioxidants, such as mitoQ and SkQ, to mitigate the decline of mitophagy and improve mitochondrial function. However, so far, human and animal trial results have been somewhat uncertain, though some small improvements have been reported in some cases.

Further down the road, therapies that directly repair mitochondria are far more preferable than compensating for their decline. Approaches such as those being developed by SENS Research Foundation as part of its MitoSENS program are the kinds of therapies we ultimately should be striving to develop, as they could potentially fix the problem entirely. Earlier this year, our community provided funding for the MitoSENS program to take this therapy to animal testing, and it is on the road towards human trials.

Conclusion

Developing robust therapies to address mitochondrial decline could have a significant impact on health, especially the health of the cardiovascular system.

Literature

[1] Liang, W. J., & Gustafsson, Å. B. (2020). The Aging Heart: Mitophagy at the Center of Rejuvenation. Frontiers in Cardiovascular Medicine, 7.

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, interviewed over 100 of the leading researchers in the field, hosted livestream events focused on aging, as well as attending various medical industry conferences. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, Swiss Monthly, 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.
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