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- The fact of the myocardium: a new approach will allow treating the kidneys and the heart at the same time
The fact of the myocardium: a new approach will allow treating the kidneys and the heart at the same time
Russian scientists have found that in kidney diseases, heart cells — cardiomyocytes — increase in size, in addition, the production of the protein nestin increases in the myocardium, one of the markers of cardiac stem cells responsible for restoring the heart muscle after damage. The researchers obtained their data on mice. They will help in the development of medicines for kidney diseases and heart failure. However, we need to confirm the effectiveness and safety of the new approach in humans, experts interviewed by Izvestia noted.
How mouse research will help treat the heart and kidneys
Researchers from Lomonosov Moscow State University have discovered a new approach to the treatment of heart diseases caused by kidney diseases. This opens the way to the creation of new drugs and therapeutic approaches that will allow treating various pathologies in a complex.
Part of the research team in the laboratory of mitochondrial Structure and function
Experts have studied what changes occur in the heart of male mice with type four renocardial syndrome. This is a disease in which chronic kidney disease, which often occurs when there is a violation of fat metabolism in the body, type 2 diabetes mellitus, high blood pressure and other diseases, can lead to heart failure. Chronic kidney disease, in turn, can develop due to obstructive nephropathy, a violation of the flow of urine that occurs when stones stand in the ureter.
As scientists told Izvestia, in response to such damage in the heart muscle (myocardium), two processes can be triggered: chronic inflammation and fibrosis (replacement of the myocardium with connective tissue) or repair with the participation of stem cells, one of the markers of which is the protein nestin.
The scientists conducted experiments on transgenic mice, which were divided into three groups: control mice with 14- and 28-day ureteral ligation. The ureter ligation was done to simulate a violation of urine flow in obstructive nephropathy.
At the end of the ureteral ligation period, the researchers determined electrocardiogram (ECG) parameters in all individuals, measured blood pressure, expression of fibrosis and inflammation markers, and analyzed the appearance and condition of nestin-positive (producing this protein) cells using confocal microscopy and other methods.
Images of left ventricular cells with different timing of ureter ligation
The experiment showed that the studied pathology in animals does not cause inflammation and fibrosis in the heart muscle. This is probably due to an increase in the number of nestin-positive cells having a phenotype (external signs) characteristic of cardiac stem cells.
— In the future, we plan to continue studying the phenotype of nestin-positive cells in different types of organs and tissues. We would like to develop a technique for isolating this type of cell in order to use them in the future for the treatment of acute ischemic injuries in various experimental models," the project leader, a researcher at the Laboratory of Mitochondrial Structure and Function at the A.N. Belozersky Research Institute of Physico—Chemical Biology at Lomonosov Moscow State University, told Izvestia. Polina Abramicheva.
New medicines based on research
Also, mice with a bandaged ureter showed an increase in the parameter that displays the period of contraction of the ventricles of the heart. Such a change may indicate hypertrophy of the heart muscle, that is, an increase in the size of myocardial cells, and is consistent with the results of microscopic examination of the myocardium in these animals.
The work shows that in kidney diseases, the amount of nestin increases as a result of damage to the heart muscle and thereby helps to restore the structure of the myocardium, Gulya Sharipova, cardiologist and therapist at the Semeynaya clinic network, told Izvestia.
"The new study will make it possible to treat not only the kidneys and the heart at the same time, but also oncological diseases in the future," she stressed.
Proposed mechanisms of cardiac hypertrophy development and potential contribution of nestin-producing cells to myocardial changes
The authors showed that with a renal problem (renocardial syndrome), the heart muscle in mice thickens, but does not overgrow with a scar. Instead, a pool of "repairers" of the heart is activated — nestin-positive progenitor cells, Albert Rizvanov, head of the Personalized Medicine Center of Excellence at Kazan (Volga Region) Federal University, explained to Izvestia. These are cells that are "younger" than mature tissue cells, but are already more specialized than stem cells. They are able to divide and produce offspring in the right direction.
— It seems that it is these progenitor cells that "turn on" their own regenerative mechanisms of the myocardium. The results of the study can form the basis of new therapeutic approaches. For example, pharmacological drugs or recombinant proteins that "wake up" such cells directly in the heart and increase its ability to repair. Or, for example, biomedical cellular products based on nestin-positive progenitors injected into the myocardium," the scientist said.
However, according to Albert Rizvanov, it is important to keep in mind the limitations. Nestin is a marker not only for the "repairers" of the heart. It is expressed in many types of body cells. This means that drugs aimed simply at activating it may turn out to be non-specific and cause side effects outside the heart. Therefore, in real therapy, point delivery systems and short-term activation will be required to affect the myocardium, rather than the entire body at once. Finally, the data has so far been obtained in mice. Before talking about medicines for humans, we need human confirmation, safety verification, and validation of nestin itself as a clinical biomarker, the expert concluded.
The study also involved employees of the Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, the Institute of Biomedical Problems of the Russian Academy of Sciences, the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences, and the Pushchino branch of the Russian Biotechnological University.
The results of the study, supported by a grant from the Russian Science Foundation (RSF), are published in the International Journal of Molecular Sciences.
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