Adipokines are currently widely studied cellular signaling proteins produced by adipose tissue and involved in various processes, including inflammation; energy and appetite modulation; lipid and glucose metabolism; insulin sensitivity; endothelial cell functioning; angiogenesis; the regulation of blood pressure; and hemostasis. The current review attempted to highlight the key functions of adipokines in the inflammatory mechanisms of obesity, its complications, and its associated diseases. An extensive search for materials on the role of adipokines in the pathogenesis of obesity was conducted online using the PubMed and Scopus databases until October 2022.

A wide variety of cell populations, including both immune and endothelial cells, participate in the pathogenesis of atherosclerosis. Among these groups, macrophages deserve special attention because different populations of them can have completely different effects on atherogenesis and inflammation in atherosclerosis. In the current review, the significance of different phenotypes of macrophages in the progression or regression of atherosclerosis will be considered, including their ability to become the foam cells and the consequences of this event, as well as their ability to create a pro-inflammatory or anti-inflammatory medium at the site of atherosclerotic lesions as a result of cytokine production. In addition, several therapeutic strategies directed to the modulation of macrophage activity, which can serve as useful ideas for future drug developments, will be considered.

Atherosclerosis is the most common cardiovascular disease and is the number one cause of death worldwide. Today, atherosclerosis is a multifactorial chronic inflammatory disease with an autoimmune component, accompanied by the accumulation of cholesterol in the vessel wall and the formation of atherosclerotic plaques, endothelial dysfunction, and chronic inflammation. In the process of accumulation of atherogenic lipids, cells of the immune system, such as monocytes, macrophages, dendritic cells, etc., play an important role, producing and/or activating the production of various cytokines—interferons, interleukins, chemokines. In this review, we have tried to summarize the most important cytokines involved in the processes of atherogenesis.

Cardiovascular diseases (CVD) and, in particular, atherosclerosis, remain the main cause of death in the world today. Unfortunately, in most cases, CVD therapy begins after the onset of clinical symptoms and is aimed at eliminating them. In this regard, early pathogenetic therapy for CVD remains an urgent problem in modern science and healthcare. Cell therapy, aimed at eliminating tissue damage underlying the pathogenesis of some pathologies, including CVD, by replacing it with various cells, is of the greatest interest. Currently, cell therapy is the most actively developed and potentially the most effective treatment strategy for CVD associated with atherosclerosis. However, this type of therapy has some limitations. In this review, we have tried to summarize the main targets of cell therapy for CVD and atherosclerosis in particular based on the analysis using the PubMed and Scopus databases up to May 2023.

Objective. The investigation of inflammatory response of immune cells is one of the most actual trends in research of autoimmune disorders including SSc. This study was aimed to investigate the inflammatory cytokines secretion and to evaluate the pro-inflammatory status of blood-derived monocytes in SSc. Methods. The study included 35 SSc and 25 heathy participants. Secretion of inflammatory cytokines TNF-α a, IL1β, CCL2 and IL8 was measured by ELISA in primary culture of monocytes/macrophages after stimulation with LPS on day 1 and 6 of incubation to assess the pro-inflammatory activation and immune tolerance of monocytes. Impaired tolerance of immune response is characterized by increased secretion of inflammatory mediators in response to re-stimulation. Results. Basal secretion of TNF-α, IL1β, CCL2 and IL8 was significantly higher in SSc patients than in healthy subjects. After the first LPS-stimulation secretion of TNF-α and IL1β, but not CCL2 and IL8 was also higher in SSc group. In 24 hours after re-stimulation, the secretion of IL1β, CCL2 and IL8, but not TNF-α increased significantly in SSc group compared to healthy control. CCL2 secretion by re-stimulated monocytes was 1.8-fold higher than in cells without re-stimulation in SSc group, that was significantly different from healthy subjects. Conclusion. The study results demonstrate pro-inflammatory activation and impaired immune tolerance of monocytes in SSc. The violation of immune response in terms of CCL2 may be an important factor of the chronification of inflammation in SSc. Thus, CCL2 should be considered as therapeutic target for the development of immunomodulatory strategies for SSc treatment.