◀ Back to APOB

APOB — EEF1A2

Text-mined interactions from Literome

Zeman et al., Cas Lek Cesk 2003 (Hyperlipoproteinemia Type V) : It is difficult to achieve satisfactory decreases of both plasma LDL-cholesterol (LDL-C) and triglycerides ( TG ) and increase of HDL-C with only single statin or fibrate treatment of patients with mixed hyperlipoproteinaemias (HLP)
, Prescrire Int 2004 (Hypercholesterolemia) : ( 7 ) In homozygous familial hypercholesterolaemia, high-dose statin and ezetimibe combination therapy reduced the LDL-cholesterol more effectively than high-dose statin alone
Scheen et al., Revue médicale de Liège 2006 (Coronary Artery Disease) : Further ongoing studies in the GALAXY clinical investigation programme should now demonstrate that rosuvastatin, the most potent statin to reduce LDL and increase HDL cholesterol, is also able to diminish the incidence of clinical outcomes, cardiovascular events in general and major coronary events in particular
Laaksonen et al., PloS one 2006 (Muscular Diseases) : Using lipidomic analysis we identified previously uncharacterized drug-specific changes in the plasma lipid profile despite similar statin induced changes in plasma LDL-cholesterol
Tokuno et al., J Atheroscler Thromb 2007 (Diabetes Mellitus, Type 2...) : Both statin and fibrate reduce the potency of atherogenic sd-LDL particles, but via different mechanisms : the former decreases total-LDL including sd-LDL, while the latter decreases sd-LDL specifically
Barter et al., J Lipid Res 2010 : The relationship between statin induced increases in HDL cholesterol ( HDL-C ) concentration and statin induced decreases in LDL cholesterol (LDL-C) is unknown
Bisoendial et al., Nat Rev Rheumatol 2010 (Arthritis, Rheumatoid...) : Currently, statin mediated reduction of LDL-cholesterol levels is considered to be the cornerstone of cardiovascular disease prevention
Barber et al., PloS one 2010 (Inflammation) : Bayesian and standard frequentist association analyses were performed on untreated and statin mediated changes in LDL-cholesterol , total cholesterol, HDL-cholesterol, and triglyceride on a total of 3932 subjects using data from three studies : Cholesterol and Pharmacogenetics ( 40 mg/day simvastatin, 6 weeks ), Pravastatin/Inflammation CRP Evaluation ( 40 mg/day pravastatin, 24 weeks ), and Treating to New Targets ( 10 mg/day atorvastatin, 8 weeks ) ... Using combined GWA analysis from three clinical trials involving nearly 4,000 individuals treated with simvastatin, pravastatin, or atorvastatin, we have identified SNPs that may be associated with variation in the magnitude of statin mediated reduction in total and LDL-cholesterol , including one in the CLMN gene for which statistical evidence for association exceeds conventional levels of genome-wide significance
Nair et al., Expert Rev Cardiovasc Ther 2010 (Coronary Artery Disease) : The mechanism for improved clinical outcomes with statins has clearly been associated with statin induced reductions in LDL
Calza et al., Drug, healthcare and patient safety 2009 : In comparative trials, across dose ranges this statin reduced low-density lipoprotein (LDL) cholesterol and total cholesterol significantly more than atorvastatin, simvastatin, and pravastatin, and triglycerides significantly more than simvastatin and pravastatin
Deshmukh et al., J Lipid Res 2012 (Diabetes Mellitus, Type 2...) : We carried out a genome-wide association study ( GWAS ) of LDL-c response to statin using data from participants in the Collaborative Atorvastatin Diabetes Study ( CARDS ; n = 1,156 ), the Anglo-Scandinavian Cardiac Outcomes Trial ( ASCOT ; n = 895 ), and the observational phase of ASCOT ( n = 651 ), all of whom were prescribed atorvastatin 10 mg
Medina et al., PLoS Genet 2012 : Thus, an unbiased filter approach based on transcriptome-wide profiling identified RHOA as a gene contributing to variation in LDL-cholesterol response to statin , illustrating the power of this approach for identifying candidate genes involved in drug response phenotypes