The aim – based on the analysis of the scientific literature focused on understanding the role of exosomes in the mechanisms of inflammation development and application of stem cells for cellular therapy in different pathological conditions, to identify and substantiate the prospects of using the exosomes as prognostic markers of a disease progression and application of their therapeutic potential in cardiovascular pathology. Global trends in the study of stem cells of different origins from the perspective of morphofunctional, molecular-genetic, cytogenetic, immunogenetic and cytological characteristics contribute significantly the development of regenerative medicine in the context of developing new methodological solutions for the use of stem cells and their components, particularly exosomes, for cell therapy of various pathological conditions. Studies show the indirect effect of exosomes on the immune response activation, coordination of cellular senescence processes and antigen presentation. There are also evidence of their impact on the structural and functional restoration of affected organs and blood vessels. The application potential of exosomes in practical medicine, particularly in the area of new approaches development to synthesize the newer biopharmaceuticals and as markers of multifactorial pathology course in conjunction with studies on the mechanisms of exosome involvement into immune processes is discussed. The study on the exosome-mediated mechanisms of inflammation in atherosclerosis is relevant, given the fact that their main physiological role is to implement the link between immunocompetent cells. Conclusions. Improving knowledge of the molecular biological mechanisms of the exosome influence on immunological processes in patients with cardiovascular pathology allows to expand the range of diagnostic and prognostic criteria for the formation of immuno-inflammatory reactions and endothelial dysfunction and to outline ways to personify the choice of therapeutic programs, which, in turn, can open approaches to develop fundamentally newer pharmaceuticals.
Regardless of the great progress in studying the heart failure (HF) pathophysiology, the question about involvement of immune cells activation, systemic inflammation, inflammatory cytokine dysregulation and endothelial dysfunction in maladaptive left ventricular (LV) remodeling in ischemic and nonischemic HF patients is still open to discussion. The aim was to study the characteristics of immunopathological reactions (immunoinflammatory and autoimmune), endothelial dysfunction and pathologic angiogenesis in maladaptive LV remodeling in ischemic and nonischemic HF patients. Materials and methods. A total of 20 healthy volunteers, 31 ischemic HF patients (group 1) and 43 nonischemic HF patients (group 2) were enrolled in the study. All the patients underwent coronarography, ventriculography, echocardigraphic examination. The main lymphocyte subset counts (flow cytometry), serum concentration of C-reactive protein (CRP), vascular endothelial growth factor A (VEGF), TNFα, endothelin-1 (enzyme-linked immunosorbent assay (ELISA)), autoantibodies to myocardium and vessels were detected. Results. Regardless of the HF etiology, all the examined patients demonstrated echocardiographic features of maladaptive LV remodeling and severe intracardiac hemodynamic disorders that was associated with immune system activation, namely increased total and subset lymphocyte counts, chronic systemic inflammation (CRP), autoimmune process with an increase in autoantibodies to myocardium and vessels, and endothelial dysfunction (increased endothelin-1 and VEGF). Under-expression of TNF-α combined with over-expression of VEGF seemed to indicate pathological angiogenesis in ischemic and nonischemic HF patients Conclusions. Significantly increased VEGF levels in heart failure patients can be considered as additional integral key marker of immune inflammation, endothelial dysfunction and pathological angiogenesis and may indicate maladaptive cardiac remodeling in severe heart failure.
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