Plasma and hepatic cholesterol and hepatic activities of 3-hydroxy-3-methylglutaryl-CoA
reductase and acyl CoA: cholesterol transferase are lower in rats fed citrus peel extract or a mixture of citrus bioflavonoids.
Regulation of the expression of the mitochondrial 3-hydroxy-3-methylglutaryl-CoA
Effects of the 3-hydroxy-3-methylglutaryl-CoA
reductase inhibitors, atorvastatin and simvastatin, on the expression of endothelin-1 and endothelial nitric oxide synthase in vascular endothelial cells.
The lobster mandibular organ produces soluble and membrane-bound forms of 3-hydroxy-3-methylglutaryl-CoA
One of the groups of medications commonly prescribed today are the 3-hydroxy-3-methylglutaryl-CoA
(HMG-CoA) reductase inhibitors or "statin" drugs.
The discovery of 3-hydroxy-3-methylglutaryl-CoA
(HMG-CoA) reductase inhibitors, called statins, was a breakthrough in the prevention of hypercholesterolemia and related diseases.
4,5) In this pathway, three molecules of acetyl-CoA condense successively to form 3-hydroxy-3-methylglutaryl-CoA
Like other statins it acts by inhibiting the rate limiting enzyme 3-hydroxy-3-methylglutaryl-CoA
(HMG-CoA) reductase, responsible for the endogenous production of cholesterol which forms an essential part of neuronal cell membranes.
Statins decrease cholesterol synthesis by inhibiting the rate-limiting enzyme, 3-hydroxy-3-methylglutaryl-CoA
(HMG-CoA) reductase, involved in the mevalonate and cholesterol synthesis (Riganti, et al.
57] Statins are synthetic agents that inhibit the rate-limiting enzyme of the mevalonate pathway, 3-hydroxy-3-methylglutaryl-CoA
reductase, thereby inhibiting cholesterol biosynthesis.
Statins are inhibitors of the rate-limiting enzyme, 3-hydroxy-3-methylglutaryl-CoA
(HMG-CoA) reductase, in cholesterol biosynthesis.
HMG-CoA reductase (or 3-hydroxy-3-methylglutaryl-CoA
reductase or HMGR) is the rate controlling enzyme (EC 1.