Biochemical and clinical consequences of inhibiting coenzyme Q 10 biosynthesis by lipid-lowering HMG-CoA reductase inhibitors (statins): A critical overview

Advances in Therapy

Volumn 15, Issue 4, 1998, Pages 218-228

  Bliznakov, Emile G ^a  

^a Biomedical Research Consultants   (United States)

Author keywords

Cardiovascular diseases; Cholesterol; Coenzyme Q 10; HMG CoA reductase inhibitors; Oxidative stress; Statins; Ubiquinone

Indexed keywords

ATORVASTATIN; CERIVASTATIN; FLUINDOSTATIN; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; MEVINOLIN; PRAVASTATIN; SIMVASTATIN; SQUALESTATIN; UNCLASSIFIED DRUG;

ANTIOXIDANT ACTIVITY; BIOAVAILABILITY; CARDIOVASCULAR DISEASE; CATARACT; CHOLESTEROL SYNTHESIS; DIET SUPPLEMENTATION; DOSE RESPONSE; DRUG EFFECT; DRUG MECHANISM; ELECTRON TRANSPORT; ENZYME INHIBITION; ENZYME SYNTHESIS; HUMAN; HYPERCHOLESTEROLEMIA; LIPID PEROXIDATION; LIVER INJURY; MUSCLE DISEASE; OXIDATIVE PHOSPHORYLATION; REVIEW;

EID: 0031690802     PISSN: 0741238X     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Review

References (3)

1. 10, and cardiovascular diseases. In: Proceedings of the 13th International Symposium on Drugs Affecting Lipid Metabolism. Symposium Abstract Book. May 30-June 3, 1998; Florence, Italy.
2. Gotto AM. Results of recent large cholesterol-lowering trials and implications for clinical management. Am J Cardiol 1997;79:1663-1666.
3. Roberts WC. The underused miracle drugs: the statin drugs are to atherosclerosis what penicillin was to infectious diseases. Am J Cardiol. 1996;78:377-378.