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Information × Registration Number 2123U009590, Article popup.category Стаття Title popup.author Chuiko N.Mankovskiy D.Kuryk O.Kisilenko O.Bazdyrev K.Verbitskiy V. popup.publication 07-07-2023 popup.source_user Національний медичний університет імені О. О. Богомольця popup.source http://ir.librarynmu.com/handle/123456789/8589 popup.publisher Світ медицини та біології. 2021. № 3 (77) Description Nowadays, there is a lot of experimental and clinical evidence that atherosclerosis is a chronic inflammatory disease with an autoimmune component. Endothelial damage causes a cascade of inflammatory reactions involving monocytes, macrophages, T-lymphocytes, and vascular smooth muscle cells. In recent years, the pathogenesis of atherosclerosis has been associated with monoclonal proliferation of smooth muscle cells. The article studies the brain arteries’ smooth muscle cells of the vascular walls in atherosclerosis in patients with ischemic stroke. It was determined that when cerebral vessels are damaged by atherosclerosis, there are subpopulations of smooth muscle cells in the vascular wall, which are characterized by the expression of desmin; smooth muscle cells are able to change their phenotype from contractile to synthetic, and this particular change in phenotype is one of the key points in the pathogenesis of atherosclerosis. This change of smooth muscle cells’ phenotype in the endarterium activates proliferation and active synthesis of the connective tissue matrix components, i. e. the modified smooth muscle cells are responsible for the fibrous plaque insula formation. popup.nrat_date 2025-06-30 Close