DC Field | Value | Language |
dc.contributor.author | Denisiuk, T. A. | - |
dc.contributor.author | Lazareva, G. A. | - |
dc.contributor.author | Provotorov, V. Y. | - |
dc.date.accessioned | 2022-05-04T11:58:35Z | - |
dc.date.available | 2022-05-04T11:58:35Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | Denisiuk, T.A. Lipid distress-syndrome and prospects of its correction by statines / T.A. Denisiuk, G.A. Lazareva, V.Y. Provotorov // Research result. Pharmacology and clinical pharmacology. - 2017. - Vol. 3, № 3.- P. 135-156. - Doi: 10.18413/2313-8971-2017-3-3-135-156. | ru |
dc.identifier.uri | http://dspace.bsu.edu.ru/handle/123456789/46581 | - |
dc.description.abstract | Endothelial dysfunction in peritonitis: The formed concept of lipid distress syndrome (LDS) allows us to develop a working hypothesis on the key role of endothelial dysfunction in the aggressive development of atherosclerosis. The role of vascular endothelium in atherosclerosis: The process of NO production from L-arginine through eNOS involving tetrahydrobiopterin (BH4) is discussed. With the degradation of BH4 along the free radical path, an "eNOS uncouplation" (uncoupled eNOS). The clinical role of statins: Statins manifests itself by inhibiting the enzyme 3-hydroxy- 3-methylglutaryl-coenzyme A (HMG-CoA reductase). Many large, randomized clinical trials have shown that lipid-lowering strategies that include statins have an anti-atherogenic potential | ru |
dc.language.iso | en | ru |
dc.subject | medicine | ru |
dc.subject | pharmacology | ru |
dc.subject | statins | ru |
dc.subject | endothelial dysfunction | ru |
dc.subject | atherosclerosis | ru |
dc.subject | endotoxin-induced pathology | ru |
dc.subject | NF-kB | ru |
dc.subject | PI3K/Akt pathways | ru |
dc.title | Lipid distress-syndrome and prospects of its correction by statines | ru |
dc.type | Article | ru |
Appears in Collections: | Vol. 3, № 3
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