期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 625, 期 -, 页码 39-53出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2017.06.001
关键词
LDL; PCSK9; IDOL; LDL receptor; Hypercholesterolemia; Statin; Inhibitors; Metabolic diseases
资金
- State of North Carolina
- BRITE Institute
- Atherotech Diagnostics Lab, Inc. (Birmingham, AL)
- Title III HBGI Integrated Biosciences Fellowship
- Golden LEAF Foundation
Heart disease ends the life of more people than any other disease in the United States. High levels of low density lipoprotein (LDL)-cholesterol cause heart diseases by increasing the formation of atherosclerotic plaques. Proprotein convertase subtilisin/kexin-9 (PCSK9) indirectly regulates plasma LDL levels by controlling the LDL receptor expression at the plasma membrane. PCSK9 also appears to modulate glucose intolerance, insulin resistance, abdominal obesity, inflammation, and hypertension. The magnitude of PCSK9's involvement in the onset of these metabolic abnormalities appears to be associated with age, sex, and ethnic background. Another regulator, the inducible degrader of the LDL receptor (IDOL), works by enhancing the ubiquitination of the LDL receptor. Herein, we will review the functions and regulatory mechanisms of PCSK9. The effects of PCSK9 on the LDL receptor, the relationship of this convertase with IDOL, and treatments currently available against hypercholesterolemia are also discussed. (C) 2017 Elsevier Inc. All rights reserved.
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