脂蛋白(a)在血管钙化中的作用机制及治疗进展

The mechanistic role of lipoprotein(a) in vascular calcification and advances in therapy

摘要:

脂蛋白(a)[Lp(a)]是一种低密度脂蛋白(LDL)样颗粒,由载脂蛋白B100(ApoB100)与载脂蛋白A(ApoA)通过共价键结合而成。近年来研究表明,Lp(a)水平升高是心血管疾病的独立危险因素,与此同时,血管钙化也会导致心血管疾病死亡率上升以及心血管事件风险增加。血管钙化是一种主动的、受高度调控的钙磷盐异常沉积于血管壁的病理过程,涉及血管平滑肌细胞(VSMC)向成骨/成软骨细胞的转分化,导致磷酸钙盐在动脉壁中积聚。现有证据表明,Lp(a)可通过多途径促进血管钙化的发生与发展,本文旨在综述Lp(a)的基本结构及其促进血管钙化的机制,并探讨其与血管钙化的关联性以及潜在的治疗进展。

Abstract:

Lipoprotein(a) [Lp(a)] is a low density lipoprotein(LDL)-like particle formed by the covalent bonding of apolipoprotein B100(ApoB100) and apolipoprotein A(ApoA). Recent studies have shown that elevated Lp(a) levels are an independent risk factor for cardiovascular diseases. At the same time, vascular calcification contributes to increased mortality from cardiovascular diseases and a higher risk of cardiovascular events. Vascular calcification is an active, highly regulated pathological process characterized by abnormal deposition of calcium-phosphate salts in the vascular wall. It involves the transdifferentiation of vascular smooth muscle cells(VSMC) into osteogenic/chondrogenic lineages, leading to the accumulation of calcium-phosphate salts in the arterial wall. Existing evidence indicates that Lp(a) promotes the initiation and progression of vascular calcification through multiple pathways. This review aims to summarize the basic structure of Lp(a) and its mechanisms in promoting vascular calcification, as well as to explore its association with vascular calcification and potential therapeutic advances.