Feng Ma, Rached Fabiana, Kontush Anatol, Chapman M John
National Institute for Health and Medical Research (INSERM), INSERM UMR 1166 ICAN, University of Pierre and Marie Curie - Paris 6, 91 Boulevard de l'Hôpital, Paris 75013, France; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, 91 Boulevard de l'Hôpital, Paris 75013, France.
Heart Institute (InCor), Medical School, University of Sao Paulo, and Albert Einstein Hospital, 44, Avenida Doutor Eneas Carvalho de Aguiar, Sao Paulo 05403-000, Brazil.
Cardiol Clin. 2018 May;36(2):193-201. doi: 10.1016/j.ccl.2017.10.001.
Apolipoprotein B-containing lipoproteins and low-density lipoprotein play a key role in atherosclerotic vascular disease. Modified forms of low-density lipoprotein drive inflammation, an integral aspect of plaque progression. High-density lipoprotein particles are equipped to protect low-density lipoprotein from enzymatic and nonenzymatic modification. Under normal conditions, high-density lipoproteins facilitate cholesterol efflux from tissues, preventing its accumulation with deleterious consequences. However, the high-density lipoprotein particles characteristic of dyslipidemic states associated with premature atherosclerosis are typically dysfunctional as a result of alteration in their metabolism and consequently their structure and composition. Such an effect indirectly enhances low-density lipoprotein atherogenicity.
含载脂蛋白B的脂蛋白和低密度脂蛋白在动脉粥样硬化性血管疾病中起关键作用。修饰形式的低密度脂蛋白会引发炎症,这是斑块进展的一个重要方面。高密度脂蛋白颗粒能够保护低密度脂蛋白免受酶促和非酶促修饰。在正常情况下,高密度脂蛋白促进胆固醇从组织中流出,防止其积累产生有害后果。然而,与早发性动脉粥样硬化相关的血脂异常状态下的高密度脂蛋白颗粒通常由于其代谢改变以及随之而来的结构和组成变化而功能失调。这种效应间接增强了低密度脂蛋白的致动脉粥样硬化性。