Cardiovascular diseases remain the leading cause of mortality worldwide, with particularly high burdens observed in countries undergoing socioeconomic transition. A growing body of evidence highlights the central role of oxidative stress in the pathogenesis of atherosclerosis, thrombosis, and related cardiovascular disorders. Selenium, an essential trace element, has attracted sustained scientific attention due to its incorporation into selenoproteins with critical antioxidant and anti-inflammatory functions. This article presents a comprehensive, integrative analysis of selenium status and its relationship with cardiovascular disease, grounded strictly in the existing scientific literature. Epidemiological patterns of cardiovascular morbidity and mortality in Eastern Europe and Central Asia, including Uzbekistan and Russia, are examined alongside ecological and nutritional determinants of selenium availability. Mechanistic pathways linking selenium-dependent antioxidant systems, particularly glutathione peroxidase, to vascular homeostasis and platelet function are discussed in depth. Methodological approaches for selenium assessment and cardiovascular epidemiology are critically analyzed, emphasizing strengths and limitations inherent in population-based research. The results synthesized from prior studies suggest that suboptimal selenium status may exacerbate oxidative stress, endothelial dysfunction, and inflammatory responses, thereby contributing to increased cardiovascular risk. However, inconsistencies across studies underscore the complexity of selenium biology, including dose-response relationships, regional variability, and interactions with lifestyle factors such as smoking. The discussion addresses theoretical implications, unresolved controversies, and directions for future research, particularly the need for context-specific nutritional strategies and carefully designed intervention studies. This article aims to provide a rigorous conceptual framework for understanding selenium’s role in cardiovascular health and to inform both scientific inquiry and public health policy.

This article presents the origin, mechanism of development of fungal and parasitic infections, and morphological changes that occur in tissues under their influence. Diseases caused by fungi and parasites are characterized by a chronic course in the human body. These pathologies cause a significant decrease in the immune system and the development of structural and functional changes in internal organs. Pathological processes accompanied by deep tissue damage play a leading role in the pathogenesis of fungal infections. In this case, as a result of chronic inflammation in the epithelium, connective tissue and internal organs, granulomas are formed, foci of necrosis appear, and destructive changes alternate with fibrosis and dystrophy. Direct mechanical damage to tissues by pathogens during parasitic invasions causes hemodynamic disorders and pathological changes in the vascular walls. Also, as a result of the specific reaction of the organism, inflammatory infiltrates rich in eosinophils are formed in the area and deep dystrophic processes develop.  In parasitic infections, special attention is paid to morphological processes that develop as a result of mechanical damage, toxic-allergic effects and immunopathological reactions. The article systematically and clearly analyzes the macro- and microscopic changes that occur in organs as a result of these infections. At the same time, the role of pathoanatomical signs in differential diagnosis and their practical significance in making an accurate clinical diagnosis are substantiated.