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首页> 外文期刊>Current opinion in lipidology >The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity
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The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity

机译：动脉中富含胆固醇的载脂蛋白B的脂蛋白在动脉粥样硬化的发病机制中的中心作用：简单的胜利

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Purpose of reviewToday, it is no longer a hypothesis, but an established fact, that increased plasma concentrations of cholesterol-rich apolipoprotein-B (apoB)-containing lipoproteins are causatively linked to atherosclerotic cardiovascular disease (ASCVD) and that lowering plasma LDL concentrations reduces cardiovascular events in humans. Here, we review evidence behind this assertion, with an emphasis on recent studies supporting the response-to-retention' model - namely, that the key initiating event in atherogenesis is the retention, or trapping, of cholesterol-rich apoB-containing lipoproteins within the arterial wall.Recent findingsNew clinical trials have shown that ezetimibe and anti-PCSK9 antibodies - both nonstatins - lower ASCVD events, and they do so to the same extent as would be expected from comparable plasma LDL lowering by a statin. These studies demonstrate beyond any doubt the causal role of apoB-containing lipoproteins in atherogenesis. In addition, recent laboratory experimentation and human Mendelian randomization studies have revealed novel information about the critical role of apoB-containing lipoproteins in atherogenesis. New information has also emerged on mechanisms for the accumulation in plasma of harmful cholesterol-rich and triglyceride-rich apoB-containing remnant lipoproteins in states of overnutrition. Like LDL, these harmful cholesterol-rich and triglyceride-rich apoB-containing remnant lipoprotein remnants become retained and modified within the arterial wall, causing atherosclerosis.SummaryLDL and other cholesterol-rich, apoB-containing lipoproteins, once they become retained and modified within the arterial wall, cause atherosclerosis. This simple, robust pathophysiologic understanding may finally allow us to eradicate ASCVD, the leading killer in the world.
机译：审查目的如今，已不再是一种假设，而是一个既定的事实，即富含胆固醇的载脂蛋白B（apoB）脂蛋白的血浆浓度升高与动脉粥样硬化性心血管疾病（ASCVD）有因果关系，降低血浆LDL浓度可降低人类的心血管事件。在这里，我们回顾了这一主张背后的证据，重点是支持“对保留的反应”模型的最新研究-即，动脉粥样硬化的关键起始事件是内含或富含胆固醇的富含apoB的脂蛋白的捕获最近的发现新的临床试验表明，依泽替米贝和抗PCSK9抗体（均为非他汀类药物）可降低ASCVD事件，其作用与通过他汀类药物降低血浆LDL所预期的程度相同。这些研究毫无疑问地证明了含apoB的脂蛋白在动脉粥样硬化中的起因作用。此外，最近的实验室实验和人类孟德尔随机研究揭示了有关含apoB的脂蛋白在动脉粥样硬化形成中的关键作用的新信息。关于营养过剩状态下有害的富含胆固醇和富含甘油三酸酯的富含apoB的残余脂蛋白在血浆中蓄积机制的新信息也已经出现。像LDL一样，这些有害的富含胆固醇和甘油三酸酯的载脂蛋白B残留脂蛋白残留物会在动脉壁内被保留和修饰，从而导致动脉粥样硬化.SummaryLDL和其他富含胆固醇的含载脂蛋白B脂蛋白一旦被保留并在脂质体内被修饰动脉壁，引起动脉硬化。这种简单而强大的病理生理学理解最终可能使我们根除世界上主要的杀手ASCVD。

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