Scientists slow down the aging process by removing the old age gene
A key part of every living cell is mitochondria, which process nutrients into ATP molecules for their growth. It turns out that these mitochondria are not only responsible for the nutrition of cells, but also for their death in the absence of food or oxygen.
When cells are aging, gaps appear in the mitochondria through which aggressive molecules from them leak into the cytoplasm of the cell and damage its DNA. At the same time, similar processes occur in young organisms, but the cells independently cope with them. In the elderly organism, the mechanism of splitting organelles occurs less efficiently - this leads to the destruction of cells.
“We found out that when old age comes, animal puffs of PUF2 protein begin to accumulate in the cells of animals, interfering with the work of the RNA molecules responsible for cleaning cells from damaged mitochondria. Accordingly, the destruction of such substances or the blocking of their work can protect a person from the decrepitude of the body. ”
David D’Amico of the Higher Polytechnic School in Lausanne.
It turned out that cell destruction processes are associated with changes in the work of the PUM2 protein - in young cells it transfers information about the synthesis of peptides from the nucleus to those parts of the cell where new proteins are collected. Whereas in the old cells, PUM2 is gathered into balls, instead of carrying information.
As a result of the experiment, Swiss biologists blocked the work of PUM2 in the DNA of mice and nematode worms. As a result, their mitochondria sharply rejuvenated - this allowed them to live much longer than their relatives.
In the future, biologists will continue experiments with PUM2. Perhaps in the future, scientists will learn to reduce the activity of this protein in old cells, which will increase the life expectancy.
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