Journal article

Publication year: 2015

Journal: Basic Research in Cardiology

Volume number: 110

Issue number: 2

ISSN: 0300-8428

eISSN: 1435-1803

Open access status: Hybrid

DOI Link: https://doi.org/10.1007/s00395-015-0463-z

Publisher: Springer

Abstract: 
The proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a promising treatment target to lower serum cholesterol, a major risk factor of cardiovascular diseases. Gain-of-function mutations of PCSK9 are associated with hypercholesterolemia and increased risk of cardiovascular events. Conversely, loss-of-function mutations cause low-plasma LDL-C levels and a reduction of cardiovascular risk without known unwanted effects on individual health. Experimental studies have revealed that PCSK9 reduces the hepatic uptake of LDL-C by increasing the endosomal and lysosomal degradation of LDL receptors (LDLR). A number of clinical studies have demonstrated that inhibition of PCSK9 alone and in addition to statins potently reduces serum LDL-C concentrations. This review summarizes the current data on the regulation of PCSK9, its molecular function in lipid homeostasis and the emerging evidence on the extra-hepatic effects of PCSK9.

Harvard Citation style: Schulz, R., Schlueter, K. and Laufs, U. (2015) Molecular and cellular function of the proprotein convertase subtilisin/kexin type 9 (PCSK9), Basic Research in Cardiology, 110(2), Article 4. https://doi.org/10.1007/s00395-015-0463-z

APA Citation style: Schulz, R., Schlueter, K., & Laufs, U. (2015). Molecular and cellular function of the proprotein convertase subtilisin/kexin type 9 (PCSK9). Basic Research in Cardiology. 110(2), Article 4. https://doi.org/10.1007/s00395-015-0463-z