Scientists in Germany are to study ways of using immortality enzymes to reverse damage caused to the heart and lungs by ageing.
The study – led by Dr Christian Baer from the Institute of Molecular and Translational Therapy Strategies of the Hannover Medical School (MHH) – aims to find a link between heart and lung diseases and age-related changes.
Scientists will study the chromosome caps called telomerases, also known as immortality enzymes.
These enzymes protect chromosomes from damage and shortening, which is how the cell retains its ability to divide and does not age.
But Baer said in a statement obtained by Newsflash: “In adults, this enzyme is usually switched off.”
He explained that after about 50 divisions, the telomerases are used up while the cell loses its ability to divide.
He added: “Telomer lengths are therefore biological markers of age.”
Previous studies have shown that reactivating immortality enzymes can help the battle against age-related diseases and protect the heart, where cells no longer divide in adults.
MHH said in a statement obtained by Newsflash: “Age is the biggest risk factor for all organ diseases, more precisely the weakening immune response and the reduced ability to regenerate.
“Regeneration processes in the body allow wounds to heal and injured or missing tissue parts to regrow.
“In old age, this ability diminishes greatly, because our body cells cannot divide indefinitely to renew damaged tissue over and over again.”
The team plans to isolate two mutant mouse models in which the biological ages of organs and the immune system within the body are different.
In the first model, biologically young animals with long telomeres will receive the bone marrow of biologically old animals with shortened telomeres, so that they end up with young organs but an artificially old immune system.
HHM said: “In the second model, it is exactly the other way around.”
The research will then put its focus on how the age of the immune system, heart and lungs, might affect the risk of heart attack and lung dysfunction.
Additionally, the researchers aim to show how acute lung damage develops when the heart is already damaged by a heart attack and what damage a heart attack exerts on a previously damaged lung.
Baer said: “In our study, we not only want to experimentally prove that heart and lung diseases actually influence each other, but also to examine the influence of telomere shortening and telomere damage in detail.
“Gene therapy with telomerase could improve the regeneration of the lungs and heart and thus increase the chances of survival in old age.”