Clin Chem Lab Med. 2014 Dec;52(12):1695-727. doi: 10.1515/cclm-2013-0358.
Research into lipoprotein metabolism has developed because understanding lipoprotein metabolism has important clinical indications. Lipoproteins are risk factors for cardiovascular disease. Recent advances include the identification of factors in the synthesis and secretion of triglyceride rich lipoproteins, chylomicrons (CM) and very low density lipoproteins (VLDL). These included the identification of microsomal transfer protein, the cotranslational targeting of apoproteinB (apoB) for degradation regulated by the availability of lipids, and the characterization of transport vesicles transporting primordial apoB containing particles to the Golgi. The lipase maturation factor 1, glycosylphosphatidylinositol-anchored high density lipoprotein binding protein 1 and an angiopoietin-like protein play a role in lipoprotein lipase (LPL)-mediated hydrolysis of secreted CMs and VLDL so that the right amount of fatty acid is delivered to the right tissue at the right time. Expression of the low density lipoprotein (LDL) receptor is regulated at both transcriptional and post-transcriptional level. Proprotein convertase subtilisin/kexin type 9 (PCSK9) has a pivotal role in the degradation of LDL receptor. Plasma remnant lipoproteins bind to specific receptors in the liver, the LDL receptor, VLDL receptor and LDL receptor-like proteins prior to removal from the plasma. Reverse cholesterol transport occurs when lipid free apoAI recruits cholesterol and phospholipid to assemble high density lipoprotein (HDL) particles. The discovery of ABC transporters (ABCA1 and ABCG1) and scavenger receptor class B type I (SR-BI) provided further information on the biogenesis of HDL. In humans HDL-cholesterol can be returned to the liver either by direct uptake by SR-BI or through cholesteryl ester transfer protein exchange of cholesteryl ester for triglycerides in apoB lipoproteins, followed by hepatic uptake of apoB containing particles. Cholesterol content in cells is regulated by several transcription factors, including the liver X receptor and sterol regulatory element binding protein. This review summarizes recent advances in knowledge of the molecular mechanisms regulating lipoprotein metabolism.
脂蛋白代谢的研究之所以得到发展,是因为了解脂蛋白代谢具有重要的临床意义。脂蛋白是心血管疾病的危险因素。最近的进展包括鉴定甘油三酯丰富的脂蛋白(乳糜微粒 (CM) 和极低密度脂蛋白 (VLDL))合成和分泌的因素。其中包括鉴定微粒体转移蛋白、载脂蛋白 B (apoB) 的共翻译靶向用于降解的脂质可用性的调节,以及运输囊泡的特征,这些囊泡将含有原始 apoB 的颗粒转运到高尔基体。脂肪酶成熟因子 1、糖基磷脂酰肌醇锚定高密度脂蛋白结合蛋白 1 和血管生成素样蛋白在脂蛋白脂肪酶 (LPL) 介导的分泌 CM 和 VLDL 的水解中发挥作用,以便在正确的时间将适量的脂肪酸递送到正确的组织中。低密度脂蛋白 (LDL) 受体的表达在转录和转录后水平受到调节。脯氨酸内切酶枯草溶菌素/克吕沃蛋白酶 9 (PCSK9) 在 LDL 受体的降解中起着关键作用。血浆残粒脂蛋白在从血浆中清除之前与肝脏中的特定受体结合,这些受体包括 LDL 受体、VLDL 受体和 LDL 受体样蛋白。当无脂载脂蛋白 AI 招募胆固醇和磷脂以组装高密度脂蛋白 (HDL) 颗粒时,就会发生胆固醇逆转运。ABC 转运蛋白 (ABCA1 和 ABCG1) 和清道夫受体 B 型 I (SR-BI) 的发现提供了关于 HDL 生物发生的进一步信息。在人类中,HDL-胆固醇可以通过 SR-BI 的直接摄取或通过载脂蛋白 B 脂蛋白中的胆固醇酯转移蛋白交换胆固醇酯和甘油三酯,然后由肝脏摄取载脂蛋白 B 含有的颗粒返回肝脏。细胞中的胆固醇含量受几种转录因子调节,包括肝 X 受体和固醇调节元件结合蛋白。本综述总结了调节脂蛋白代谢的分子机制的最新进展。
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