4.7 Review

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

Journal

CLINICA CHIMICA ACTA
Volume 483, Issue -, Pages 192-196

Publisher

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

Funding

  1. National Natural Science Foundation of China [81770454]
  2. Natural Science Foundation of Hunan province [2018JJ2343, 2015JJ4097]
  3. Key Project of the Education Department of Hunan Province [15A137]
  4. Visiting Scholar Foundation of Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education [CQKLBST-2014-002, CQKLBST-2015-004]
  5. Hunan Province

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available