How Japanese reverse aging process in cells?
It is common knowledge in the aging field that mutations in the DNA can lead to aging. This is one long held theory of aging. This view is easy to understand when
One realizes that DNA is the blue print for making our proteins and thus DNA regulates all cell functions. Mutations in the DNA therefore lead to unregulated functions, i.e., aging. For this and many other reasons, the DNA damages that accumulate throughout our lifespan have been viewed as a hallmark of aging.
The Theory Of Aging Start With The DNA We Carry
Most of our DNA is located in the nucleus of our cells; however, DNA is also located in other cellular places. Our mitochondria, the organelle in charge of producing energy, has its own DNA and is therefore also suspected to be involved in the aging process. Mutation accumulations in the mitochondrion are easy to envision when one keeps in mind that as the mitochondria produces energy in the form of ATP, it also produces via side reactions, reactive oxygen species (ROS). And ROS, like all free radicals, can lead to uncontrolled and harmful reactions that damage not only the mitochondria but also all other molecules in the cells including proteins and the DNA in the nucleus.
The Mitochondria In Our Cells And Theory Of Aging
There is no doubt that the mitochondrion plays a role in aging as studies that entail modifying proteins in the mitochondria lead to accelerated aging. However, the mechanisms for how the aging process is promoted by the mitochondrion are still being elucidated and many questions remain. For example, all mitochondria have multiple copies of its DNA. So the redundancy of the DNA may mean that the damage caused by ROS can be kept in check for many years. This observation brings into question how ROS is actually affecting the mitochondria. Another interesting observation is that genetically modified mice that either have increased antioxidant defenses do not extend lifespan or experiments that artificially increase ROS do not show increased aging. So how do we
The Japanese Flip The Mutation Theory Of Aging Around
In the article by Hashizume and his colleagues, the researcher may have come up with a reason for how mitochondria DNA is affecting aging (Scientific Reports, 5:10434). This research group looked not at the genetic mutations sequences but rather how the DNA was being modified without changing the DNA sequence, which is commonly referred as epigenetic modifications. In other words in epigenetics, the DNA can be “modified” by several mechanisms including, for example, adding a methyl group to the DNA.
It’s Not Mitochondrial Mutations
The DNA base pair sequence is not changed therefore it is technically NOT mutated but it is modified and the response is that proteins and their function can be regulated in a positive or negative way. These epigenetic changes have been well-documented and recognized as part of aging and are viewed as another hallmark of aging. Here is what is novel about this article.
The Mitochondrial Mutation Theory Of Aging Challenged
Since the DNA is not mutated, it is therefore technically possible that if we can find a way to reverse the epigenetic modification on the DNA, the process would reverse the aging modification on the mitochondria DNA. And that is exactly what these researchers have done.
Proof Using Young And Old Cells
Using fibroblast cells, the researchers were able to change the epigenetic modifications and essentially reverse the aging process on these cells and rejuvenate them.
So the researchers have demonstrated that it is not the mutations in the mitochondria that lead to aging but rather the epigenetics changes. But not only that, it can be reversed. In addition, they also determine that the mitochondria DNA sequences that are of particular importance in terms of affecting the aging epigenetic signature, was a sequence that encodes for protein (product of GCAT gene) required to make glycine, an amino acid common in all proteins.
Resveratrol Regulates A Main Epigenetic Protein
Interestingly to those taking resveratrol is the following. Resveratrol regulates sirtuin 3, which is the MAIN deacetylating sirtuin (i.e., another epigenetic modifying protein) found in the mitochondria. Sirtuin 3 has already been shown to modify ROS and enzymes involved with energy metabolism. So it would be interesting in the future to determine if sirtuin 3 can also affect the production of glycine and improve our cells and hence our lifespans too.
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