The Key to Reversing Aging: Folded Mitochondria?

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Getting older is a fact of life. As we age, we can grow bigger, smarter and stronger. But at a certain point, our bodies often start to slow down. The idea behind why we age and why our bodies slow down is that we start to lose the ability to make enough energy to support all the different functions that our body carries out.

Hazel H. Szeto, MD, PhD, is a medical doctor and a research scientist. She may have found the answer to reversing the aging process by restoring a person’s ability to make energy. Szeto presented her work last month at Experimental Biology 2021

To better understand Szeto’s discovery, we must first understand how the body makes energy. We produce energy in the form of a small molecule called adenosine triphosphate, or ATP. When ATP is broken down, it releases energy that allows our bodies to do work, such as contracting the muscles in our arms and legs so we can lift a box. Mitochondria are small structures in the cells that make ATP from the food we eat.

Some cells (such as those in the liver) have hundreds to thousands of mitochondria, where others (such as blood cells) have no mitochondria at all. Mitochondria are usually bean-shaped. They contain an inner membrane that has folds—called cristae—like an accordion. Special proteins on the cristae create ATP. The membrane is folded to increase the amount of surface area so that ATP can be made in a very small space. If you could straighten out the inner membranes of all of the mitochondria in your body, it would cover about 11 Olympic-size pools!

As we age, we lose cristae in our mitochondria. The cristae straighten out, and the ATP-making proteins can’t come together to make ATP. And, our cells can’t make as much energy as before. Scientists have found that this loss of cristae happens when we lose cardiolipin, a type of fat in our blood. Cardiolipin keeps the membrane folded and the cristae intact.

Szeto is trying to prevent cardiolipin from being destroyed during the aging process so that cristae is not lost. Her research has shown that treating old mice with an antioxidant molecule increased cardiolipin and cristae in the mitochondria of their hearts and eyes. This caused the old mice to produce just as much ATP as younger mice. Szeto also found that the muscles of these old mice became stronger and that age-related heart and eye damage was reversed.

This treatment has not been used in people yet, but it could be the answer for many age-related diseases and injuries such as heart disease. Szeto’s research shows that the basic understanding of how our body works—or doesn’t work—is very important in finding ways to keep ourselves healthy as we age.

Dao H. Ho, PhD, is a biomedical research physiologist at Tripler Army Medical Center in Honolulu. She served as a meeting blogger for the American Physiological Society’s 2021 annual meeting at Experimental Biology. The views expressed in this blog post are those of the author and do not reflect the official policy or position of the U.S. Department of the Army, U.S. Department of Defense or the U.S. government.

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