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Please use this identifier to cite or link to this item: http://dspace.bsu.edu.ru/handle/123456789/46595
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dc.contributor.authorRagulina, V. A.-
dc.contributor.authorKostina, D. A.-
dc.contributor.authorDovgan, A. P.-
dc.contributor.authorBurda, Y. E.-
dc.contributor.authorNadezhdin, S. V.-
dc.date.accessioned2022-05-04T16:25:23Z-
dc.date.available2022-05-04T16:25:23Z-
dc.date.issued2017-
dc.identifier.citationNuclear factor kappa B as a potential target for pharmacological correction endothelium-associated pathology / V. A. Ragulina [et al.] // Research result. Pharmacology and clinical pharmacology. - 2017. - Vol. 3, № 1.- P. 114-124. - Doi: 10.18413/2500-235X-2017-3-1-114-124. - Refer.: p. 120-124.ru
dc.identifier.urihttp://dspace.bsu.edu.ru/handle/123456789/46595-
dc.description.abstractThe nuclear factor kappa B (NF-κB) is one of transcription factors. A high interest in studying the biological role of the signal system and its contribution to the development of cardiovascular, oncological and autoimmune diseases is obvious. A number of stimuli (proinflammatory cytokines: tumor necrosis factor α, interleukin 1β, ligand CD40 and others) trigger the canonical and non-canonical pathways of NF-κB signaling, which increase the expression of genes regulating synthesis of cytokines and chemokines, cell proliferation and differentiation, angiogenesis, immune reactions and apoptosis. However, pathological activation of NF-κB violates the balance of substances participating in the normal activity of the cardiovascular system. This leads to the development and progression of endothelium-associated pathology and comorbidityru
dc.language.isoenru
dc.subjectmedicineru
dc.subjectpharmacologyru
dc.subjectnuclear factor kappa Bru
dc.subjectNF-κBru
dc.subjectendothelial dysfunctionru
dc.subjectischemia-reperfusionru
dc.subjectpharmacological correctionru
dc.subjectcomorbidityru
dc.titleNuclear factor kappa B as a potential target for pharmacological correction endothelium-associated pathologyru
dc.typeArticleru
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