Scientists at the University of Tsukuba have discovered that aging of human cells can be slowed down or even reversed. They identified two genes whose functioning is associated with aging mechanisms. The cells of our body receive energy from the mitochondria living inside the organelles . Apparently, at the dawn of evolution, anaerobic cells, unable to assimilate oxygen, united in symbiotic cooperation with ancient bacteria that could do this. As a result, today mitochondria are no longer independent organisms, and serve as a source of energy for cells.
A popular theory of aging is that due to the constant division of mitochondria in cells, there is a gradual accumulation of mitochondrial DNA mutations. Mitochondria “deteriorate” and their energetic properties come to naught. Soon after the appearance of the mitochondrial theory of aging, a theory was proposed according to which the presence of free radicals in the body affects the “damage” of mitochondria. But at the moment, quite a lot of research is citing evidence against the radical theory. But scientists from Tsukuba believe that perhaps the point is not that mitochondrial DNA deteriorates, but that over time certain genes begin to turn on and off. Under the guidance of Professor Jun-Ichi Hayashi, the researchers were able to switch some genes to the “youthful” position and thus reverse the aging process. In their study, scientists compared fibroblasts, cells of human connective tissue, in children under the age of 12 and in the elderly from 80 to 97 years. Naturally, in older organisms, a significant decrease in cellular respiration was observed . This is a set of biochemical reactions that take place in the cells of living organisms, during which carbohydrates, lipids and amino acids are oxidized to carbon dioxide and water. However, the scientists did not see any signs that the DNA was damaged more in the cells of the elderly than in the younger ones.
The researchers suggested that epigenetic effects take place here – processes that change the physical structure of DNA, as a result of which some genes are turned on or off, but at the same time they do not change its very sequence. This means that it is theoretically possible to reverse epigenetic changes in DNA by reprogramming cells for this. Scientists reprogrammed the cells they took into the state of stem cells, and then turned them back into fibroblasts. As a result, it turned out that cellular respiration in all cells was restored to the level of young ones. Therefore, researchers began looking for genes that could be switched in order to prevent the above defects from occurring. They found two genes, GCAT and SHMT2, that regulate the synthesis of glycine , an amino acid produced by mitochondria. It was found that by regulating the work of these genes, it is possible to completely restore the normal functioning of mitochondria in cells. And the addition of glycine to the cells of elderly people for a period of 10 days led to a complete restoration of cellular respiration of fibroblasts. It follows from the study that, in contrast to the existing theory of aging, defects in cellular respiration of fibroblasts arise due to epigenetic processes. Is it possible by regulating these processes to control human aging? This will need to be established – and if successful, it will be possible to develop glycine therapy to combat aging.