Suppr超能文献

[脂蛋白脂肪酶(LPL)在动脉粥样硬化发病机制中的作用]

[Lipoprotein lipase (LPL) in the pathogenesis of atherosclerosis].

作者信息

Skoczyńska A

机构信息

Klinika Chorób Wewnetrznych i Zawodowych, Akademii Medycznej we Wrocławiu.

出版信息

Postepy Hig Med Dosw. 1998;52(4):347-65.

PMID:9780756
Abstract

The role of lipoprotein lipase (LPL) in the development of atheromatosis is subject of the increased interest for about 20 years, since then Zilversmit observed that LPL activity is found in greater amounts in atherosclerotic than normal arteries. The general action of this enzyme is hydrolysis of triglycerides in triglyceride rich lipoproteins and thus regulation of metabolism of circulating as well antiatherogenic as proatherogenic lipoproteins. The effect of LPL on the biology of arterial wall seems to be atherogenic. The mechanisms of this effect of LPL is 1) augmentation of the adhesion and aggregation of LDL; 2) influence on the oxygen modification of LDL and increased uptake of oxy-LDL by macrophages; 3) dysfunction of endothelial barrier and retention of atherogenic lipoproteins in the arterial wall and 4) the activity of LPL macrophage origin. Possible atherogenic actions of LPL based on in vitro experimental studies are reviewed.

摘要

脂蛋白脂肪酶(LPL)在动脉粥样硬化形成过程中的作用在大约20年里一直备受关注,自齐尔弗斯米特观察到在动脉粥样硬化动脉中发现的LPL活性比正常动脉中更多以来。这种酶的一般作用是水解富含甘油三酯的脂蛋白中的甘油三酯,从而调节循环中抗动脉粥样硬化和促动脉粥样硬化脂蛋白的代谢。LPL对动脉壁生物学的影响似乎具有致动脉粥样硬化性。LPL这种作用的机制是:1)增强低密度脂蛋白(LDL)的黏附和聚集;2)影响LDL的氧化修饰并增加巨噬细胞对氧化型LDL(oxy-LDL)的摄取;3)内皮屏障功能障碍以及致动脉粥样硬化脂蛋白在动脉壁中的滞留;4)巨噬细胞来源的LPL的活性。本文综述了基于体外实验研究的LPL可能的致动脉粥样硬化作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验