Low-Density Lipoprotein Receptor-Dependent and Low-Density Lipoprotein Receptor-Independent Mechanisms of Cyclosporin A-Induced Dyslipidemia

Author(s):
Kockx, M.; Glaros, E.; Leung, B.; Ng, T.W.; Berbee, J.F.P.; Deswaerte, V.; Nawara, D.; Quinn, C.; Rye, K.A.; Jessup, W.; Rensen, P.C.N. (0000-0002-8455-4988); Meikle, P.J.; Kritharides, L.
Published
2016
Publication type
Article / Letter to editor

Abstract

Conclusions-We demonstrate that CsA does not cause hyperlipidemia via direct effects on the LDLr. Rather, LDLr deficiency plays an important permissive role for CsA-induced hyperlipidemia, which is associated with abnormal lipoprotein clearance, decreased lipoprotein lipase activity, and increased levels of apolipoprotein C-III and proprotein convertase subtilisin/kexin type 9. Enhancing LDLr and lipoprotein lipase activity and decreasing apolipoprotein C-III and proprotein convertase subtilisin/kexin type 9 levels may therefore provide attractive treatment targets for patients with hyperlipidemia receiving CsA.

apolipoprotein C-IIIcyclosporin Ahyperlipidemiaimmunosuppressionlipolysisproprotein convertase subtilisin/kexin type 9triglycerides
Date issued
2016-06-01
Language
English
Publisher
LIPPINCOTT WILLIAMS & WILKINS
Is part of
Arteriosclerosis, Thrombosis, and Vascular Biology (2016), Vol. 36, no. 7, p. 1338-+
hdl
1887/99415
doi
10.1161/ATVBAHA.115.307030