Dear readers

Before the 10th anniversary of the Cardiometry journal, the pulse of the time and the expansion of the space of scientific interests for our readers, who play a major role in the life and development of our Journal, are becoming more and more remarkable. One can easily notice the qualitative difference between the numbers of the Journal, which, like the lighthouse, dictates the direction of further advance, i.e. provides a wide variety of topics for issues, creating a systematic collection of scientific papers. Maintaining this tradition, in this issue of our Journal we will focus on one of, perhaps, the most trending areas in modern cardiology and oncology.

The 21st century boldly announced itself by penetrating into the holy of holies: the compartmentalization of intracellular structures – mitochondria, and has already accumulated scientific evidence data confirming their unique role in the regulation of energy metabolism, stem cell differentiation, proliferation, migration, apoptosis and necrosis. It is known that under conditions of high loads, mitochondria carry out the process of complex formation of large associates, transfer from one cell to another, retaining the mitochondrial DNA code. Recent evidence has shown that the physiological properties of healthy mitochondria provide their ability to replace damaged mitochondria, suggesting that replacing damaged mitochondria with healthy ones may protect cells from their further pathological changes. Moreover, mitochondria can also be actively released into the extracellular space and potentially be transferred from cell to cell in the central nervous system. This enhanced interest in mitochondrial therapy calls for a better understanding of the mechanisms responsible for the mitochondrial transport, absorption, and cellular defense, especially in human diseases such as cardiovascular disease, metabolic syndrome, neurodegenerative diseases, immune system disorders, and cancer.

Recently, mitochondrial transplantation has attracted the attention of many scientists. Mitochondrial transplantation is considered as a potential therapeutic method that can be used to treat specific diseases associated with the mitochondrial dysfunction or mtDNA damage. Previous studies have shown that isolated mitochondria from various sources, including cultured stem cells or autologous tissues, yield successful results in damaged tissues, organs, or cells due to the development of mitochondrial therapy approaches.

In a series of papers presented by us herein, we review the latest information on the involvement of mitochondria in the mechanisms of malignant transformation, mitochondrial dynamics of metabolic programming, on the features of mitochondrial transplantation in vitro and in vivo in models of ischemic reperfusion injury of the heart, the lungs, the spinal cord, and the liver. Our another article, devoted to some biological effects of mitochondrial therapy, shows the possibility of preventing the development of myocardial infarction and blocking the metastatic activity of melanoma B16 in mice with intraperitoneal transplantation of intact heart mitochondria against the background of chronic neurogenic pain. The heart is an organ with high energy requirements, and therefore it is not surprising that mitochondria occupy 30% of the total volume of cardiomyocytes and generate approximately 95% of ATP in the organism. However, in order to understand how the structure of the myocardium changes in an extreme situation, when we deal with an interference of pathological processes (a bi-model system of chronic neurogenic pain and the melanoma growth), a morphological analysis of the heart muscle was carried out and a real structural catastrophe was revealed, demonstrating deep damage caused to cardiomyocytes. One more article herein intentionally precedes the paper discussing the structural catastrophe in order to present some the results of a symmetrical study during experimental mitochondrial therapy, where one can visually verify the possibility of preventing ischemic damage and necrosis of the heart tissue using intraperitoneal transplantation of live mitochondria.

In this issue of the Journal, you will get acquainted with the results of mitochondrial therapy using allogeneic liver mitochondria in the BALB/c Nude mice with B16/F10 melanoma and slowing the tumor growth in mice of both sexes. In the context of the tumor growth, the study of mitochondrial dysfunction will provide a deeper understanding of the critical problems of cancer. The obtained knowledge of the state of mitochondria in pathologically altered cells, the degree of their dysfunction provide essential information for understanding the pathophysiology of cancer, which gives impetus to the development of mitochondrial pharmacology. In this regard, the data from the articles on the content of cAMP in the mitochondria of the heart cells and serum in the C57BL/6 mice with growing B16/F10 melanoma, linked to chronic neurogenic pain, may be very useful.

Concluding our short guided tour of the pages of this issue, we hope it would be enjoyable, and we wish the attentive readers to find that trickle of information that will satisfy his/her interest to some extent.