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Inflammatory Stress Induces Statin Resistance by Disrupting 3-Hydroxy-3-Methylglutaryl-CoA Reductase Feedback Regulation
Author(s) -
Yaxi Chen,
Halcyon Ku,
Lei Zhao,
David C. Wheeler,
LungChih Li,
Qing Li,
Zac Varghese,
John F. Moorhead,
Stephen H. Powis,
Ailong Huang,
Xiong Z. Ruan
Publication year - 2013
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.113.301301
Subject(s) - sterol regulatory element binding protein , hmg coa reductase , vascular smooth muscle , endocrinology , atorvastatin , medicine , sterol , cholesterol , biology , cholesteryl ester , cd36 , pharmacology , chemistry , reductase , biochemistry , lipoprotein , receptor , enzyme , smooth muscle
The risk of cardiovascular disease is increased by up to 33 to 50× in chronic inflammatory states and convention doses of statins may not provide the same cardiovascular protection as in noninflamed patients. This study investigated whether the increase in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCoA-R)-mediated cholesterol synthesis observed under inflammatory stress was resistant to the action of statins and if so, whether this was because of interference with the sterol regulatory element binding protein cleavage-activating protein pathway.

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