BSMU scientists have developed a drug candidate for the treatment of coronary heart disease

An interdisciplinary team from Bashkir State Medical University and Hangzhou Pedagogical University (China) has created a fundamentally new candidate compound for the treatment of acute myocardial infarction, which works not with vessels, but with heart cells.

The study is in great demand: heart attack remains one of the main causes of death and disability in the world. Current therapies effectively restore blood flow in blocked vessels. However, even after a successful operation, long-term risks remain high.

In the first stage, scientists have created a molecule that reduces the area of cardiac tissue death. This discovery promises serious prospects: improved forecasts, accelerated rehabilitation and reduced risk of complications. Recently, the team moved to a new frontier — during testing on biological models, the effectiveness of the molecule was confirmed. Using microscopy, chemiluminescence and immunohistochemistry, carried out on the basis of the morphological laboratory of the Institute of Fundamental Medicine of the BSMU, the researchers recorded a significant decrease in the zone of damage to the heart muscle in laboratory animals.

"In our laboratory, it was proved that the use of deubiquitinating enzymes has a positive effect on the survival of cardiomyocytes," Vlas Shchekin, head of the morphological laboratory at the Institute of Fundamental Medicine of the BSMU said .

Unlike traditional therapy aimed at eliminating blood clots and restoring blood circulation in the heart muscle, the new molecule works differently: it protects cardiomyocytes - the main cells of the heart muscle at that critical moment when blood flow is restored. It is then that the so-called reperfusion damage occurs: the return of oxygen inflicts an additional blow on the cells. The new molecule "calms down" damaged tissues and prevents the cell self-destruction program from starting.

"The reason for the development of myocardial infarction is the cessation of blood supply to the area of the heart muscle due to the blockage of coronary vessels with a thrombus or a fragment of atherosclerotic plaque, which leads to its death. Current treatment aims to restore blood flow through a variety of treatments. But here the paradox lies: the return of blood to damaged tissue itself inflicts an additional blow to cells - reperfusion damage. With the help of this molecule (compound), we found a way to integrate into the internal mechanisms of cellular death of the heart muscle, to "calm down" damaged tissues at the very critical moment when blood flow is restored," - Anton Tyurin, head of the Department of Internal Diseases of the BSMU of the Ministry of Health of Russia.

The focus of the researchers is the ubiquitin protein. The team found that reducing its activity in the ischemic zone dramatically increased cell survival. Deubiquitinating enzymes play a key role here — scientists call them a new and promising target for drug effects.

Project manager, MD, Professor Alexander Samorodov emphasizes that the new development does not cancel the existing methods, but complements them. The task of the future drug is to make the restoration of blood flow safe for tissues. So that after placing the stent or dissolving the thrombus, the heart muscle remains as alive and efficient as possible. This is a fundamentally different, deeper level of infarction therapy.

The development was carried out in the laboratory of small targeted molecules of BSMU (Interuniversity Student Campus) as part of an international grant with the support of the State Natural Science Foundation of China (NSFC) and the Russian Science Foundation. The project is dedicated to "Evaluation of the role of deubiquitinating enzymes in ischemic-reperfusion myocardial injury and the creation of cardioprotective agents."

In the near future - clinical trials. If they are successful, the developed compound will become the basis of the first in its class cardioprotector, which will protect the heart not at the level of blood vessels, but at the level of cells.