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[动脉粥样硬化形成的近期病理生理学方面]

[Recent pathophysiologic aspects of atherogenesis].

作者信息

Kostner G

机构信息

Institut für Medizinische Biochemie, Universität Graz.

出版信息

Wien Med Wochenschr. 1990 Feb 28;140(4):101-9.

PMID:2158191
Abstract

Although the causes for atherogenesis are multifactorial, derangements of the lipid- and lipoprotein metabolism play a key role for the development of early lesions. The major risk factor for atherosclerosis cholesterol is a substance necessary for life. Cholesterol may be synthesized by any living cell of the human body. In order to save body fuel, cells take up cholesterol from circulation. All plasma lipids are bound in the blood to specific apolipoproteins. Apo-B containing lipoproteins are capable in binding to specific cell surface receptors (B/E-R) and to ingest cholesterol into the cells. Under circumstances, where the binding affinity to the B/E-R is reduced, atherogenic lipoproteins accumulate in the plasma and are eventually cleared by the scavenger receptor. These mechanisms play a key role in atherogenesis. Apo-A containing lipoproteins in contrast are designed to shuttle deposited cholesterol from the periphery to the liver, where it is oxidized to bile acids. The role of the four cell types:endothelial- and smooth muscle cells, macrophages and thrombocytes for atherogenesis in the concert with pathophysiological events of the lipid metabolism are discussed, and genetic diseases are explained at a molecular level.

摘要

尽管动脉粥样硬化的病因是多因素的,但脂质和脂蛋白代谢紊乱在早期病变的发展中起关键作用。动脉粥样硬化的主要危险因素胆固醇是生命必需的物质。人体的任何活细胞都可以合成胆固醇。为了节省身体能量,细胞从循环中摄取胆固醇。所有血浆脂质在血液中都与特定的载脂蛋白结合。含载脂蛋白B的脂蛋白能够与特定的细胞表面受体(B/E-R)结合,并将胆固醇摄入细胞。在某些情况下,当与B/E-R的结合亲和力降低时,致动脉粥样硬化脂蛋白在血浆中积聚,最终被清道夫受体清除。这些机制在动脉粥样硬化的发生中起关键作用。相比之下,含载脂蛋白A的脂蛋白旨在将沉积的胆固醇从外周转运到肝脏,在那里它被氧化成胆汁酸。本文讨论了四种细胞类型:内皮细胞和平滑肌细胞、巨噬细胞和血小板在脂质代谢的病理生理事件协同作用下对动脉粥样硬化的作用,并在分子水平上解释了遗传疾病。

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