Scientists were able to prevent the aging of the heart, suppressing the activity of one of proteins.
Biologists from the National centre for cardiovascular research found that telomeres — the protective end parts of chromosomes in the cells of the myocardium in mice rapidly shorten with age, impairing cardiac function. Scientists were able to prevent the aging of the heart, suppressing the activity of one of proteins. The study is published in the Journal of Cell Biology.
Newborn mice can effectively repair damaged heart muscle, however, the Mature rodent heart attacks cause irreversible damage, heart failure and death. With age, cardiomiocity — heart muscle cells — emerge from the cell cycle, limiting their reproduction and regenerative functions.
Scientists decided to test whether telomere length with aging of kardiomiotsitov. The researchers found that the chromosome ends are shortened rapidly during the first weeks after birth of mice. This coincided with a decrease in the synthesis of telomerase, the enzyme that restores telomeres. Eventually switched cellular system, prevent DNA damage by inhibiting growth and reproduction of cells. A key component of the system is a protein-inhibitor P21.
Biologists have used genetically modified mice whose cells were unable to produce enough telomerase. In animals, the telomeres were even shorter than that of conventional rodents, and their cationicity continued to proliferate after day after birth.
If, however, suppress the activity of the P21 protein, this prolongs the ability of kardiomiotsitov to growth and reproduction, allowing the mice weeks of age to more effectively regenerate damaged cardiac tissue. Scientists are also working to create animals with increased synthesis of the enzyme and to test whether the lengthening of telomeres on the successful recovery of kardiomiotsitov.
