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Pol. Merkur. Lek (Pol. Med. J.), 2017, XLII/249: 125-128 Maximize

Pol. Merkur. Lek (Pol. Med. J.), 2017, XLII/249: 125-128

Title: The inflammatory processes in atherogenesis 

Authors: Cichoń N, Lach D, Dziedzic A, Bijak M, Saluk J. 

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SUMMARY IN POLISH & ENGLISH. FULL ARTICLE ONLY IN POLISH.

The inflammatory processes in atherogenesis


Cichoń N, Lach D, Dziedzic A, Bijak M, Saluk J.

Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Poland

Atherogenesis is the process of atherosclerotic plaque formation, leading to coronary artery heart disease. This process involves immune cells, mainly T and B cells, monocytes and macrophages. The process of atherogenesis is induced by inflammatory damage of endothelial cells. The characteristic construction features of the atherosclerotic plaque is a predisposing factor for acute coronary syndromes. The accumulation of inflammatory cells in the artery inner membrane enhances the local inflammatory process due to the secretion of reactive oxygen species, inflammatory cytokines and metalloproteinases, which accelerate the development of atherosclerotic lesions in the arteries. In chronic inflammation of endothelial cells, which is atherosclerosis, there is a decrease in the concentration of elastin and collagen as a result of the increased apoptosis of smooth muscle cells of the intima. This reduces the integrity and strength of the fibrous cap that covers a layer of thrombogenic plaque from contact with blood elements. Permanent inflammation promotes the formation of necrotic core, composed of dead smooth muscle cells, macrophages and foam cells formed by phagocytosis of oxidized lipid molecules. The thin fibrous cap and a large necrotic core are the cause of plaque rupture and thrombus formation within the coronary artery.

Key words: atherogenesis, atherosclerotic plaque, inflammatory mediators

Pol Med J, 2017; XLII (249); 125–128