Cardiovascular and pulmonary diseases are closely linked. MHH researchers now want to demonstrate the molecular mechanisms and investigate the influence of age-related changes in the heart, lungs and immune system.
Cardiovascular diseases and lower respiratory tract diseases are among the most common causes of death, especially in older people. Epidemiological studies examining the incidence and distribution of disease demonstrate a close link between cardiovascular and pulmonary disease. However, little is known about the molecular biological causes.
A research team led by Professor Dr. Christian Bär from the Institute of Molecular and Translational Therapy Strategies at Hannover Medical School (MHH) now wants to investigate the mechanisms involved in the interaction between heart and lung disease and the influence of age-related changes.
Reduced regeneration at the short ends of the chromosome
Acute lung damage or acute respiratory distress syndrome increases the risk of heart attack. On the other hand, a heart attack or chronic heart failure can lead to acute lung problems. Age is the biggest risk factor for all organ diseases, more precisely the weakening of the immune response and the reduction of regeneration capacity. Regeneration processes in the body allow wounds to heal and injured or missing tissue parts to grow back.
In old age, this ability greatly diminishes because our body’s cells cannot divide endlessly to renew damaged tissue over and over again. The reason for this is the so-called telomeres, the ends of chromosomes. Genetic information is stored in chromosomes. With each cell division, the telomeres shorten a little. After about 50 divisions, they run out, so to speak, and the cell completely loses its ability to divide. “Telomere lengths are therefore biological markers of age”, explains Professor Bär.
Chimeric mouse models with different organs and immune ages
The research team will first investigate the role of immune and organ aging in the heart and lungs. For this, two genetically different mouse models are produced, called chimeric, in which the biological ages of the organs and the immune system within the body are different. Biologically young animals with long telomeres receive bone marrow from biologically old animals with shortened telomeres, so they now have young organs but an artificially old immune system. In the second model, it is exactly the opposite.
The researchers then want to test how the age of the immune system, as well as the heart and lungs, affects a heart attack and lung damage. In addition, they want to demonstrate how acute lung damage develops when the heart is already damaged by a heart attack and what damage a heart attack does to a previously damaged lung. “In our study, we not only want to experimentally prove that heart and lung diseases really influence each other, but also examine the influence of telomere shortening and telomere damage in detail,” says Professor Bär.
Gene therapy may improve organ regeneration
The studies are also intended to lay the groundwork for new therapies. The focus is on telomerase. The enzyme protects the ends of chromosomes from damage and shortening. In this way, the cell retains its ability to divide and does not age. Therefore, telomerase is also known as the “immortality enzyme” and is the subject of anti-aging research.
“In adults, this enzyme is usually turned off,” explains Professor Baer. In previous studies, the scientist had already found that the reactivation of telomerase helps against age-related diseases and protects the heart. Although heart muscle cells no longer divide in adults, the enzyme apparently detoxifies the cells and thus improves heart function. “Gene therapy with telomerase could improve the regeneration of the lungs and heart and thus increase the chances of survival in old age”, suggests the molecular biologist.
Provided by Hannover Medical School
Quote: Exploring the Role of Organ and Immune Aging in Heart and Lung Disease (2023, Jan 24) Retrieved Jan 24, 2023 from https://phys.org/news/2023-01-exploring-role-immune- aging-heart.html
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