Lipoprotein(a) and inhibitors of proprotein convertase subtilisin/kexin type 9

被引：31
|
作者：
Kotani, Kazuhiko [1 ]
Banach, Maciej [2 ]
机构：
[1] Jichi Med Univ, Div Community & Family Med, Shimotsuke, Tochigi, Japan
[2] Med Univ Lodz, Chair Nephrol & Hypertens, Dept Hypertens, Lodz, Poland
来源：
JOURNAL OF THORACIC DISEASE | 2017年 / 9卷 / 01期
关键词：
Apolipoprotein(a) [apo(a); apolipoprotein B (apoB); familiar hypercholesterolemia; LDL receptor; LDL receptor-related protein (LRP); scavenger receptor (SR); FAMILIAL HYPERCHOLESTEROLEMIA; RECEPTOR; RISK; DISEASE; METAANALYSIS; CATABOLISM; THERAPY; PCSK9; METABOLISM; PHASE-1;
D O I：
10.21037/jtd.2017.01.40
中图分类号：
R56 [呼吸系及胸部疾病];
学科分类号：
摘要：
Lipoprotein(a) [Lp(a)] has been identified as a risk factor for cardiovascular disease. Lp(a) levels are also high under certain clinical conditions, including familial hypercholesterolemia and high blood low-density lipoprotein (LDL) cholesterol levels. Few effective generic therapies for modulating Lp(a) have been developed. However, new therapies involving inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9) using monoclonal antibodies have markedly reduced the blood LDL levels-and the Lp(a) levels as well. Much attention has therefore been focused on this therapy and its utility. The mechanism by which PCSK9 inhibitors reduce the Lp(a) levels remains unclear. We here describe the effects of PCSK9 inhibitors on Lp(a) and discuss potential mechanisms and perspectives of this topic.
引用
收藏
页码：E78 / E82
页数：5
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