GENOMIC FACTORS (TOLL-LIKE RECEPTORS GENES) IN DEVELOPMENT OF ATHEROSCLEROSIS AND ITS CLINICAL MANIFESTATIONS

Development of atherosclerosis and its clinical manifestations, i.e. unstable angina, myocardial infarction, and ischemic stroke, is largely determined by a genetic inheritance, particularly inherited variation of the genes encoding Toll-like receptors (TLRs), a major effector of innate immune syste...

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Autores principales: I. I. Zhidkova, A. V. Ponasenko, M. V. Khutornaya, A. G. Kutikhin, O. L. Barbarash
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Lenguaje:RU
Publicado: SPb RAACI 2017
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spelling oai:doaj.org-article:2c0a14e9f0644449987c80fc1e88a8e32021-11-18T08:03:46ZGENOMIC FACTORS (TOLL-LIKE RECEPTORS GENES) IN DEVELOPMENT OF ATHEROSCLEROSIS AND ITS CLINICAL MANIFESTATIONS1563-06252313-741X10.15789/1563-0625-2017-3-241-254https://doaj.org/article/2c0a14e9f0644449987c80fc1e88a8e32017-07-01T00:00:00Zhttps://www.mimmun.ru/mimmun/article/view/1258https://doaj.org/toc/1563-0625https://doaj.org/toc/2313-741XDevelopment of atherosclerosis and its clinical manifestations, i.e. unstable angina, myocardial infarction, and ischemic stroke, is largely determined by a genetic inheritance, particularly inherited variation of the genes encoding Toll-like receptors (TLRs), a major effector of innate immune system. Polymorphisms of the TLR genes may affect vascular inflammation, as well as plaque formation and its stability. Miriades of immune cells and bioactive substances are involved into pathogenesis of atherosclerosis. They exert different effects upon vascular wall and participate in development of universal inflammatory response. Local inflammatory reaction underlyes atherosclerotic plaque destabilization and endothelial dysfunction. This response is associated with TLR activation and induced synthesis of proinflammatory cytokines. Here we review the literature on the role of inherited variations within the TLR genes in the development and progression of atherosclerosis and its complications. Moreoxer, we conclude that a search for genomic markers of atherosclerosis, e.g., TLR gene polymorphisms, may be applied in personalized cardiovascular medicine, in order to predict clinical course and evolution of the disorder, like as to perform prophylactic measures aimed for prevention of the disease progression.I. I. ZhidkovaA. V. PonasenkoM. V. KhutornayaA. G. KutikhinO. L. BarbarashSPb RAACIarticleatherosclerosisgene polymorphismstoll-like receptorsallelic variantsinnate immune receptorsinflammationimmune responseImmunologic diseases. AllergyRC581-607RUMedicinskaâ Immunologiâ, Vol 19, Iss 3, Pp 241-254 (2017)
institution DOAJ
collection DOAJ
language RU
topic atherosclerosis
gene polymorphisms
toll-like receptors
allelic variants
innate immune receptors
inflammation
immune response
Immunologic diseases. Allergy
RC581-607
spellingShingle atherosclerosis
gene polymorphisms
toll-like receptors
allelic variants
innate immune receptors
inflammation
immune response
Immunologic diseases. Allergy
RC581-607
I. I. Zhidkova
A. V. Ponasenko
M. V. Khutornaya
A. G. Kutikhin
O. L. Barbarash
GENOMIC FACTORS (TOLL-LIKE RECEPTORS GENES) IN DEVELOPMENT OF ATHEROSCLEROSIS AND ITS CLINICAL MANIFESTATIONS
description Development of atherosclerosis and its clinical manifestations, i.e. unstable angina, myocardial infarction, and ischemic stroke, is largely determined by a genetic inheritance, particularly inherited variation of the genes encoding Toll-like receptors (TLRs), a major effector of innate immune system. Polymorphisms of the TLR genes may affect vascular inflammation, as well as plaque formation and its stability. Miriades of immune cells and bioactive substances are involved into pathogenesis of atherosclerosis. They exert different effects upon vascular wall and participate in development of universal inflammatory response. Local inflammatory reaction underlyes atherosclerotic plaque destabilization and endothelial dysfunction. This response is associated with TLR activation and induced synthesis of proinflammatory cytokines. Here we review the literature on the role of inherited variations within the TLR genes in the development and progression of atherosclerosis and its complications. Moreoxer, we conclude that a search for genomic markers of atherosclerosis, e.g., TLR gene polymorphisms, may be applied in personalized cardiovascular medicine, in order to predict clinical course and evolution of the disorder, like as to perform prophylactic measures aimed for prevention of the disease progression.
format article
author I. I. Zhidkova
A. V. Ponasenko
M. V. Khutornaya
A. G. Kutikhin
O. L. Barbarash
author_facet I. I. Zhidkova
A. V. Ponasenko
M. V. Khutornaya
A. G. Kutikhin
O. L. Barbarash
author_sort I. I. Zhidkova
title GENOMIC FACTORS (TOLL-LIKE RECEPTORS GENES) IN DEVELOPMENT OF ATHEROSCLEROSIS AND ITS CLINICAL MANIFESTATIONS
title_short GENOMIC FACTORS (TOLL-LIKE RECEPTORS GENES) IN DEVELOPMENT OF ATHEROSCLEROSIS AND ITS CLINICAL MANIFESTATIONS
title_full GENOMIC FACTORS (TOLL-LIKE RECEPTORS GENES) IN DEVELOPMENT OF ATHEROSCLEROSIS AND ITS CLINICAL MANIFESTATIONS
title_fullStr GENOMIC FACTORS (TOLL-LIKE RECEPTORS GENES) IN DEVELOPMENT OF ATHEROSCLEROSIS AND ITS CLINICAL MANIFESTATIONS
title_full_unstemmed GENOMIC FACTORS (TOLL-LIKE RECEPTORS GENES) IN DEVELOPMENT OF ATHEROSCLEROSIS AND ITS CLINICAL MANIFESTATIONS
title_sort genomic factors (toll-like receptors genes) in development of atherosclerosis and its clinical manifestations
publisher SPb RAACI
publishDate 2017
url https://doaj.org/article/2c0a14e9f0644449987c80fc1e88a8e3
work_keys_str_mv AT iizhidkova genomicfactorstolllikereceptorsgenesindevelopmentofatherosclerosisanditsclinicalmanifestations
AT avponasenko genomicfactorstolllikereceptorsgenesindevelopmentofatherosclerosisanditsclinicalmanifestations
AT mvkhutornaya genomicfactorstolllikereceptorsgenesindevelopmentofatherosclerosisanditsclinicalmanifestations
AT agkutikhin genomicfactorstolllikereceptorsgenesindevelopmentofatherosclerosisanditsclinicalmanifestations
AT olbarbarash genomicfactorstolllikereceptorsgenesindevelopmentofatherosclerosisanditsclinicalmanifestations
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