PCSK9: A potential regulator of apoE/apoER2 against inflammation in atherosclerosis?

Xue-Qin Bai, Juan Peng, Mei-Mei Wang, Jun Xiao, Qiong Xiang, Zhong Ren, Hong-Yan Wen, Zhi-Sheng Jiang, Zhi-Han Tang, Lu-Shan Liu

Journal: Clinica chimica acta; international journal of clinical chemistry 2018;483():192-196

PMID: 29727700

Full Text on Elsevier Science View on PubMed

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.

Address: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang 421001, China.; The Department of Pediatrics, The Nanhua Affiliated Hospital, University of South China, Hengyang 421001, China.; Medical College, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.; Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang 421001, China. Electronic address: [email protected].; Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang 421001, China. Electronic address: [email protected].

DOI: 10.1016/j.cca.2018.04.040