Reiner Z, Tedeschi-Reiner E
Medicinskog fakulteta Sveucilista u Zagrebu, Klinickog odjela Zavoda za opću patolosku fiziologiju KBC Rebro.
Lijec Vjesn. 1990 May-Jun;112(5-6):175-82.
The authors present an up-to-date review on etiopathogenesis of atherosclerosis. Theories of etiology of atherosclerosis are described: response-to-injury hypothesis, lipid deposition hypothesis, lysosome hypothesis, encrustation hypothesis, mural thrombi hypothesis, monoclonal and clonal senescence hypothesis. The role of endothelial injury and platelet adhesion as well as smooth muscle cells proliferation due to these events, their growth control and the role of macrophages in atherogenesis are explained thoroughly. Special attention is focused on the interaction of arterial cells and lipoproteins at sites of vessel injury, lipid metabolism of the lesion and on synergy of arterial injury caused by various injury mechanisms and hypercholesterolemia in atherogenesis. Atherosclerotic risk factors and their impact on atherogenesis are discussed as well (e.g. hyperlipoproteinemia, hypertension, tobacco smoking, diabetes and abnormal glucose tolerance, gout, obesity, menopause and oral contraceptives, diminished physical activity, type A of personality behavior etc.). The possibilities of regression or reversal of ateromatous plaques are presented too.
作者们对动脉粥样硬化的病因发病机制进行了最新综述。描述了动脉粥样硬化的病因理论：损伤反应假说、脂质沉积假说、溶酶体假说、结壳假说、壁血栓假说、单克隆和克隆衰老假说。详细解释了内皮损伤和血小板黏附的作用，以及这些事件导致的平滑肌细胞增殖、它们的生长控制和巨噬细胞在动脉粥样硬化形成中的作用。特别关注血管损伤部位动脉细胞与脂蛋白的相互作用、病变的脂质代谢，以及各种损伤机制和高胆固醇血症在动脉粥样硬化形成中引起的动脉损伤协同作用。还讨论了动脉粥样硬化的危险因素及其对动脉粥样硬化形成的影响（如高脂蛋白血症、高血压、吸烟、糖尿病和糖耐量异常、痛风、肥胖、绝经和口服避孕药、体力活动减少、A型人格行为等）。还介绍了动脉粥样斑块消退或逆转的可能性。
