Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 1.736
5-Year Impact Factor – 2.135
Index Copernicus  – 168.52
MEiN – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

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Advances in Clinical and Experimental Medicine

2006, vol. 15, nr 6, November-December, p. 971–978

Publication type: editorial article

Language: English

Adhesion Molecules, Cytokines and Endothelial Dysfunction in Atherosclerosis

Molekuły adhezyjne, cytokiny i zaburzenie funkcji śródbłonka w miażdżycy

Kinga Musiał1,, Danuta Zwolińska1,

1 Department of Pediatric Nephrology, Silesian Piasts University of Medicine in Wrocław, Poland

Abstract

The aim of this review is to present current knowledge of atherosclerosis. Recent investigations point to chronic inflammation as a key player in the functional impairment of the endothelium. Enhanced cell migration and diapedesis lead to monocyte recruitment and their change into macrophages, thus initiating atherosclerotic plaque formation. The involvement of adhesion molecules, interleukins, growth factors, and enzymes in the adhesion cascade is tightly connected with dyslipidemia and the overproduction of reactive oxygen species. The latter may be a causative factor for the propagation of endothelial damage due to pleiotropic activities, including the impact on lipid metabolism, adhesion cascade functioning, cytokine activity, and nitric oxide bioavailability. The over−activity of pro−atherogenic agents results in a vicious circle of tissue destruction. These self−perpetuating reactions progressively impair the function of vessels, resulting in lumen occlusion, local ischemia, and clinical complications. Therefore, clarifying the mechanisms responsible for atherosclerosis seems to be the key target for future investigations.

Streszczenie

Celem pracy jest przedstawienie obecnego stanu wiedzy na temat miażdżycy. Badania ostatnich lat wskazują na rolę przewlekłego procesu zapalnego jako kluczowego czynnika zaburzającego funkcję śródbłonka. Nasilona migracja i diapedeza komórek prowadzi do gromadzenia monocytów i przekształcania w makrofagi, co jest początkiem procesu tworzenia blaszki miażdżycowej. Udział molekuł adhezyjnych, interleukin, czynników wzrostu i enzymów w kaskadzie adhezji jest ściśle związany z zaburzeniami gospodarki lipidowej i wydzielaniem wolnych rodników tlenowych. Procesy wolnorodnikowe mogą powodować postępującą destrukcję śródbłonka przez wielokierunkowe oddziaływania, m.in. na metabolizm lipidów, kaskadę adhezji, aktywność cytokin i biodostępność tlenku azotu. Wzmożona aktywność czynników proaterogennych uruchamia błędne koło niszczenia tkanek. Nieodwracalne reakcje stopniowo zaburzają funkcję naczyń, powodując zwężenie ich światła, niedokrwienie i powikłania. Wyjaśnienie mechanizmów odpowiedzialnych za rozwój miażdżycy wymaga więc dalszych badań.

Key words

adhesion molecules, cytokines, nitric oxide, reactive oxygen species, endothelium

Słowa kluczowe

molekuły adhezyjne, cytokiny, tlenek azotu, wolne rodniki tlenowe, śródbłonek

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