ZAPALJENSKI PROCES U ATEROGENEZI: NOVE ČINJENICE O STAROM PLAMENU.

INFLAMMATORY PROCESS IN ATHEROGENESIS: NEW FACTS ABOUT OLD FLAME.

Introduction. Atherosclerosis is a progressive, multifactorial, diffuse, multisystemic, chronic, inflammatory disease, which is manifested by disorders of vascular, immune and metabolic system. Pathogenesis of this disease is not fully understood. Endothelial Dysfunction and Inflammatory Process. Endothelial dysfunction is recognized as the crucial step in atherogenesis. A lot of studies have confirmed the involvement of various mediators of inflammation in initial proatherogenic processes, such as the upregulation of adhesion molecules on endothelial cells, binding of low density lipoproteins to endothelium, activation of macrophages and proliferation of vascular smooth muscle cells. Fatty stain and Inflammatory Process. Fatty stain consists of foam cell accumulation. After foam cell formation, mediators of inflammation initiate a series of intracellular events that include the induction of inflammatory cytokines. Thus, a vicious circle of inflammation, modification of lipoproteins and further inflammation can be maintained in the artery. Transitory Lesion and Inflammatory Process. In transitory lesion intensive phagocytosis of oxidized low density lipoproteins additionally activates monocytes and macrophages and consequently facilitates and exacerbates the inflammatory response. Fibrotic Plaque and Inflammatory Process. Inflammatory process, matrix-degrading metalloproteinases activity, platelets aggregation and smooth muscle cells proliferation play a central role in development of fibrotic plaque. Complex Lesion and Inflammatory Process. It has been shown that inflammation is closely related to the development of atherosclerotic plaque rupture. Conclusion. The contribution of inflammatory process has become increasingly meaningful in understanding the initiation, progression and clinical manifestations of atherosclerosis. [ABSTRACT FROM AUTHOR]

Uvod. Ateroskleroza je progresivna, višefaktorska, difuzna, multisistemska, hronična, zapaljenska bolest kod koje postoji poremećaj vaskularnog, imunskog i metaboličkog sistema. Aterogeneza nije do kraja razjašnjena. Disfunkcija endotela i inflamacija. Ono što se sa sigurnošću zna jeste da disfunkcija endotela ima bitnu ulogu u aterogenezi. Mnoge studije su potvrdile ulogu različitih medijatora zapaljenja u početnim proaterogenskim procesima, kao što su regulacija adhezije molekula za endotelne ćelije, vezivanje lipoproteina male gustine za endotelijum, aktivacija makrofaga i proliferacija vaskularnih ćelija glatkih mišića. Masna mrlja i inflamacija. Masna mrlja, koja se razvija na području endotelne disfunkcije, sastoji se od akumulacije penastih ćelija. Nakon stvaranja penastih ćelija, medijatori zapaljenja iniciraju seriju intracelularnih događaja koji uključuju indukciju inflamacijskih citokina. Tako se može održati začarani krug zapaljenja, modifikacije lipoproteina i daljeg zapaljenja u arteriji. Tranzitorna lezija i inflamacija. U tranzitornoj leziji pojačana fagocitoza oksidizovanih lipoproteina male gustine dodatno aktivira monocite i makrofage i samim tim olakšava i pogoršava inflamacijsku reakciju. Fibrozni plak i inflamacija. Inflamacijski proces, aktivnost metaloproteinaza koje razgrađuju matriks, agregacija trombocita i proliferacija ćelija glatkih mišića imaju glavnu ulogu u razvoju fibroznog plaka. Komplikovana lezija i inflamacija. Dokazano je da je zapaljenje tesno povezano s razvojem rupture aterosklerotičnog plaka. Zaključak. Sve je jasniji doprinos inflamacijskog procesa za razumevanje nastajanja, napredovanja i kliničkih manifestacija ateroskleroze. [ABSTRACT FROM AUTHOR]

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