Journal
CLINICA CHIMICA ACTA
Volume 483, Issue -, Pages 192-196Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.cca.2018.04.040
Keywords
Proprotein convertase subtilisin kexin 9; Atherosclerosis; Inflammation; Apolipoprotein E; Apolipoprotein E receptor 2
Categories
Funding
- National Natural Science Foundation of China [81770454]
- Natural Science Foundation of Hunan province [2018JJ2343, 2015JJ4097]
- Key Project of the Education Department of Hunan Province [15A137]
- Visiting Scholar Foundation of Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education [CQKLBST-2014-002, CQKLBST-2015-004]
- Hunan Province
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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.
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