Home > Journals > Italian Journal of Vascular and Endovascular Surgery > Past Issues > Giornale Italiano di Chirurgia Vascolare 1998 March;5(1) > Giornale Italiano di Chirurgia Vascolare 1998 March;5(1):9-19



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Giornale Italiano di Chirurgia Vascolare 1998 March;5(1):9-19


language: English, Italian

Atherosclerosis. Lipid metabolism and molecular changes in the arterial wall

Petruzzo P., Brotzu G.

From the Department of Surgical Sciences and Organ Transplantation Chair of Vascular Surgery University of Cagliari, Cagliari, Italy


Atherosclerosis (ATS) is a progressive disease of blood vessels that causes clinical events particularly in late adulthood. Although atherosclerotic lesions are present in children there is a close correlationship between age and incidence and severity of ATS. Infrarenal abdominal aorta, iliofemoral vessels, carotid bifurcation and coronary arteries are particularly susceptible while other sites are relatively “resistant”. Although findings tend to establish close correlation between plaque localization and geometric configuration of the vessels, the mechanism which underlie the role of flow characteristics in atherogenesis remains to be clarified. The initiating event in ATS lesions formation is considered to be a multifactorial injury to the endothelial lining: the different forms of insult determine an inflammatory response, a protective fibroproliferative reaction which becomes excessive over many years. ATS lesions are characterized by different cellular composition and interactions: macrophages, T-lymphocytes, smooth muscle cells have been found in the core of ATS lesions, but also platelets and endothelial cells play an important role in the development of ATS plaque as well as cytokines and regulator growth factors. In the lesioned areas it has been shown an increase in lipid content, particularly cholesteryl esters, especially in the areas where endothelial regrowth has occurred. The accumulation of lipid depends on alterations within the vessel wall also without increase in plasma lipid levels. These findings suggest an increased uptake of lipid, LDL, by regenerating endothelium or an increase of endogenous synthesis and/or esterification of cholesterol in the proliferating cells of the arterial wall. Endothelial cells can modify LDL into oxLDL to make them recognizable to the scavanger receptors of monocytes which then fagocyte them. The increased uptake and metabolism of LDL may be related to the metabolic requirements of the arterial wall cells to proliferate. In fact, recent studies have evidenced a possible role of the MDR-1 gene (multi drug resistance), which codifies the P-glycoprotein, correlated to cholesterol transport towards the rough endoplasmic reticulum where it is esterified by ACAT enzyme. MDR-1 gene is usually expressed in human arterial walls and its expression seems to be directly correlated to the age and the presence of ATS plaques.

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