"Mens sana in corpore sano" is the famous aphorism of the ancient Roman poet Juvenal, which means "A sound mind in a healthy body".

Even the ancients noticed the relationship between physical health and the health of our minds.

Modern scientists from the Johns Hopkins University (USA) have discovered that the BDNF protein literally links these two components of human health.

A new study, published in the journal Proceedings of the National Academy of Sciences, found that this protein, known as a natural antidepressant, not only promotes learning and memorizing, stimulates the growth of nerve cells, improves blood vessel function, but also maintains heart muscle health.

Scientists conducted a series of experiments in mice and myocardial cells grown in the laboratory. The results showed that the multi-tasking protein BDNF (brain-derived neurotrophic factor) helps the cells of the heart muscle to contract and relax, which contributes to the prolongation of the life of the heart. Protein BDNF provides a cascade of biochemical reactions in the heart tissue, the violation of which is associated with a risk of heart failure.

Heart failure is a very serious problem for modern healthcare. For example, in the United States, about 6 million people live with this disease, and on a global scale the number of such patients exceeds 23 million! The results of the new study may help to find new approaches to the treatment of certain types of heart failure.

One multitasking protein affects the functions of many organs.

The BDNF protein is known to scientists due to the ability to combat depressive conditions and stimulate the growth of nerve cells (hence its name). The researchers suggest that between depression and heart failure have a certain biochemical link because both diseases often go in tandem.

Dr. Ning Feng, a leading author of the latest work, an expert in cardiology from the Johns Hopkins School of Medicine in Baltimore, says: "Our data not only recalled the incredible complexity of the chemistry and physiology of the heart, but also gave us another example of the ability of one multifunctional protein act on several fronts and influence the functions of many organs and systems ".

The results also provided a good explanation for the fact that in many patients with heart failure the level of BDNF protein in the blood is below normal. It used to be a mystery to researchers.

"We showed that BDNF directly controls the ability of cardiomyocytes (cardiac muscle cells) to contract correctly. This sheds light on why many people with heart failure and reduced tolerance to physical activity have lowered the level of this substance, "said the co-author of the work, Dr. Nazareno Paolocci, a professor of medicine at Johns Hopkins.

In the course of their experiments, scientists subjected the heart of rodents in vivo and isolated cells of the heart muscle to the effect of the BDNF protein. Myocardial cells taken from healthy mice responded with an improvement in the contractile function in the presence of BDNF. But cells from animals with severe heart failure, even if they were treated with a solution of BDNF, answered very little or did not respond at all.

It's all about the presence of TrkB receptors on the surface of the heart cells that react to the presence of the BDNF protein. TrkB receptors in mice with a normal heart differed from TrkB receptors in their diseased relatives. The main difference was that they reacted better to BDNF and passed this protein more actively into the cell.

Ineffective variant of TrkB receptors weaker response to BDNF. This variant of the receptor is quite common, and its presence suggests a tendency to heart disease. Because of it in critical situations, the heart reacts worse to the stimulating protein.

Genetically modified mice with an ineffective variant of TrkB from birth had a somewhat worse function of the heart - it decreased less, pumped blood less efficiently, and required more time to relax after each stroke.

Dr. Feng says: "Summing up what has been said, it turns out that the interaction of BDNF and its receptor is the key to a cascade of biochemical reactions on which the health of the heart muscle depends".

Disorders of BDNF-TrkB interaction and heart failure in chemotherapy.

Scientists came to another important conclusion. Disruption of BDNF-TrkB communication explains why heart failure may occur with cancer chemotherapy. Some chemopreparations block a variety of cellular receptors, among which TrkB. Of course, this is necessary to stop the growth of cancer cells. But here lies the cause of side effects.

The researchers also proved that the low level of BDNF protein alone is not enough for the development of heart failure. For this, chronic deficiency or insensitivity to BDNF should be combined with other pathological factors - then the development of the disease is possible.

"Without chronic stressors such as hypertension or increased cardiac muscle load, deficiency of BDNF protein can not cause a complete picture of the disease, but it creates favorable conditions for its development," concluded Professor Paolozzi.

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