Lilit M. Sukiasyan

Numerous studies addressing the fundamental aspects of atherosclerosis emphasize the importance of systematically organizing the accumulated data. The second part of this lecture provides an analysis of the critical mechanisms involved in the development of atherosclerosis. This analysis includes a discussion on the roles of inflammasomes, hemodynamic disorders within the vascular wall, vasa vasorum pathology, endothelial cell dysfunction, matrix metalloproteinases, and the Notch and Wnt signaling pathways in the process of atherogenesis. Additionally, it explores the specific characteristics of the pathogenesis of vascular calcification associated with atherosclerosis. A dedicated section thoroughly reviews contemporary pharmacotherapeutic strategies for managing atherogenic dyslipidemia. A comprehensive analysis of current concepts regarding the pathogenesis of atherosclerosis, along with promising approaches to drug therapy, will facilitate the identification of future research directions within the field of lipidology. This endeavor has the potential to elevate preventive cardiology to a new standard.

Atherosclerosis and atherosclerosis-related cardiovascular diseases are a significant public health concern and a rapidly evolving area of research in both fundamental and clinical medicine. Despite the extensive history of studying, many aspects of atherosclerosis etiology and pathogenesis remain unclear. Traditionally, the pathogenesis of atherosclerosis has been viewed in terms of the localized accumulation of specific lipoprotein fractions in the arterial wall. However, both innate and adaptive immunity play active roles in atherogenesis. Cells and mediators of the immune system engage in intricate interactions with cellular and extracellular components in all layers of the vascular wall. For this reason, scientific community have reached a consensus on the crucial role of inflammation in the onset, progression, and destabilization of an atherosclerotic plaque. Therefore, atherogenesis can be considered not only as a metabolic disorder, but also as an immunoinflammatory process. The aim of this lecture was to summarize contemporary data regarding the role of inflammation at various stages of the atherosclerotic continuum.

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are now uncovering new possibilities in the field of internal medicine owing to their diverse protective effects. In the second part of the literature review, we explore potential applications of SGLT2i in hepatology, neurology, ophthalmology, and oncology, mechanisms of action of such drugs as dapagliflozin, empagliflozin, canagliflozin, etc, and their effect on different organs and systems.

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have emerged as a revolutionary class of drugs with far-reaching protective effects in multiple organs. The protective potential of SGLT2i is much broader than that of the classical concept of glucose control and consists of an entire conglomerate of associated pleiotropic effects. This study aims to provide a descriptive review of the pleiotropic therapeutic potential of SGLT2i. The first part of the literature review examined the use of SGLT2i in cardiology and nephrology. The use of SGLT2i represents an innovative approach to improving patients’ quality of life and course of heart failure and chronic kidney disease, regardless of left ventricular ejection fraction and type 2 diabetes.

Galantamine, a centrally-acting acetylcholinesterase (AChE) inhibitor, is currently used as a first-line therapy for the symptomatic treatment of Alzheimer’s disease. Long-term consumption of sugar-rich beverages has been shown to be associated with the development of various clinical conditions, including metabolic syndrome, impaired cholinergic transmission, and cognitive decline. The aim of this study was to determine the effect of long-term fructose consumption on changes in short-term plasticity (STP) parameters of rat brain lateral entorhinal cortex (lEC) neurons during high-frequency stimulation (HFS) of the cholinergic nucleus basalis magnocellularis (NBM) and to evaluate the therapeutic potential of Galantamine in neurodegeneration induced by diabetes. Using the method of determining AChE activity in brain slices from intact rats exposed to Galantamine, we revealed that AChE activity showed a declining trend in the NBM and lEC. Our findings indicated that STP changes were observed in the fructose group and were associated with degenerative disorders. Specifically, there was a dramatic decrease in the proportion and intensity of excitatory responses during HFS as well as a significant increase in the mean frequency of background spike activity in neuronal populations with all response types. Galantamine resulted in a recovery tendency for the balance and intensity of excitatory and inhibitory responses. A characteristic feature of the therapeutic effect of Galantamine is an increase in the share and expression of responses in the neuronal population, exhibiting tetanic depression and post-tetanic potentiation to NBM stimulation. This clearly indicates that these neurons play a key role in homeostatic plasticity and integration into neuronal chains of cholinergic projections.