| Literature DB >> 29727700 |
Xue-Qin Bai1, Juan Peng1, Mei-Mei Wang2, Jun Xiao1, Qiong Xiang1, Zhong Ren1, Hong-Yan Wen3, Zhi-Sheng Jiang1, Zhi-Han Tang4, Lu-Shan Liu5.
Abstract
Atherosclerosis is characterized by chronic inflammation and lipid accumulation in arterial walls, resulting in several vascular events. Proprotein convertase subtilisin kexin 9 (PCSK9), a serine protease, has a pivotal role in the degradation of hepatic low-density lipoprotein receptor (LDLR). It can increase plasma concentrations of low-density lipoprotein cholesterol and affect lipid metabolism. Recently, PCSK9 has been found to accelerate atherosclerosis via mechanisms apart from that involving the degradation of LDLR, with an emerging role in regulating the inflammatory response in atherosclerosis. Apolipoprotein E receptor 2 (apoER2), one of the LDLR family members expressed in macrophages, can bind to its ligand apolipoprotein E (apoE), exhibiting an anti-inflammatory role in atherosclerosis. Evidence suggests that apoER2 is a target of PCSK9. This review aims to discuss PCSK9 as a potential regulator of apoE/apoER2 against inflammation in atherosclerosis.Entities:
Keywords: Apolipoprotein E; Apolipoprotein E receptor 2; Atherosclerosis; Inflammation; Proprotein convertase subtilisin kexin 9
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Year: 2018 PMID: 29727700 DOI: 10.1016/j.cca.2018.04.040
Source DB: PubMed Journal: Clin Chim Acta ISSN: 0009-8981 Impact factor: 3.786