TY - JOUR A2 - 江贤成AU - 爪夷，Motasim M. AU - 弗罗利希，吉日AU - 陈森美Y. PY - 2020 DA - 2020年2月1日TI - 脂蛋白（a）叛军：新洞察结构，功能，代谢，致病性，和药物影响脂蛋白（a）分子SP - 3491764 VL - 2020 AB - 脂蛋白（a）[脂蛋白（a）]，又名“LP少了”，在60年代被发现挪威医生卡尔·伯格的实验室。从那时起，我们已经大大提高了我们的血脂和心血管疾病（CVD）的知识。脂蛋白（a）是一个神秘类脂蛋白的被排他地形成在肝脏和包括两个主要部件，载脂蛋白（APO）B100（APO-B100）的单个副本拴的蛋白质的单拷贝表示为载脂蛋白（a）中的apo（a）中。脂蛋白（a）的血浆水平在出生后的生活在短短几个月内很快提高到一个稳定的浓度。In adults, Lp(a) levels range widely from <2 to 2500 mg/L. Evidence that elevated Lp(a) levels >300 mg/L contribute to CVD is significant. The improvement of isoform-independent assays, together with the insight from epidemiologic studies, meta-analyses, genome-wide association studies, and Mendelian randomization studies, has established Lp(a) as the single most common independent genetically inherited causal risk factor for CVD. This breakthrough elevated Lp(a) from a biomarker of atherosclerotic risk to a target of therapy. With the emergence of promising second-generation antisense therapy, we hope that we can answer the question of whether Lp(a) is ready for prime-time clinic use. In this review, we present an update on the metabolism, pathophysiology, and current/future medical interventions for high levels of Lp(a). SN - 2090-3030 UR - https://doi.org/10.1155/2020/3491764 DO - 10.1155/2020/3491764 JF - Journal of Lipids PB - Hindawi KW - ER -