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Сурункали гиперкалорияли овқатланиш билан индукция қилинган атеросклерозда эндотелиал дисфункция ривожланишининг молекуляр механизмлари

Samandar GanievTashkent State University of EconomicsAkmaljon AzamatjonovStudent, Faculty of General Medicine No. 2 , Tashkent State Medical UniversityRavshan KhusanovDiyorbek ErgashboevStudent, Faculty of General Medicine No. 2 , Tashkent State Medical UniversityХамид МатюсуповTashkent State Medical University Kimyo International University in Tashkent Republican Specialized Scientific and Practical Medical Center of Oncology and RadiologySamandar GanievАкмалжон АзаматжоновРавшан ҲусановPhD, доцент, кардиолог, кардиореаниматолог высшей квалификации, Ташкентский международный университет КимёДиёрбек ЭргашбоевHamid MatyusupovSamandar GanievАкмалжон АзаматжоновРавшан ҲусановPhD, доцент, кардиолог, кардиореаниматолог высшей квалификации, Ташкентский международный университет КимёДиёрбек ЭргашбоевHamid Matyusupov
2026ru
ABI

Annotatsiya

This article investigates the molecular mechanisms of endothelial dysfunction in atherosclerosis developing in the context of chronic hypercaloric intake. Excess energy consumption was shown to be associated with the development of insulin resistance, dyslipidemia, low-grade inflammation, and oxidative stress, which together create the pathobiological basis of atherogenesis. Based on clinical and laboratory analysis, it was established that, as vascular injury becomes more severe, endothelium-dependent vasodilation decreases, while markers of structural and functional vascular wall damage, including CIMT, ADMA, and endothelin-1, increase. Correlation analysis confirmed a close relationship between the severity of atherosclerosis, the degree of metabolic disturbances, and the extent of endothelial dysfunction. The findings emphasize the pathogenetic importance of dietary correction, body weight control, and the management of cardiovascular risk factors in the prevention and slowing of atherosclerosis progression.

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