[Pharmacogenetics and anti-inflammatory effect of HMG-CoA reductase inhibitors].
Atherosclerosis is a result from the association of lipid deposition in the arterial wall and inflammatory process. This inflammatory process may be detected by clinical markers of systemic inflammation, such as ultrasensible C-reactive protein, which is associated with cardiovascular risk, independently of lipid levels. Statins reduce the inflammation associated to atherosclerosis, which may be verified by a reduction of the C-reactive protein levels. It seems that statins alter immune function by modulating post-translational protein prenylation. Individual genetic variations are associated with modulation of statins lipid-lowering effect; however, few studies have related the effect of the genetic variants with anti-inflammatory effect of statins. In addition to the genes involved in the cholesterol metabolism, genetic factors affecting statins pharmacodynamics and/or pharmacokinetics are potentially responsible for lipid and anti-inflammatory effects.
Laboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Criciúma, SC.
Alexandre B
AB
Rosendo
Felipe
F
Dal-Pizzol
Marilu
M
Fiegenbaum
Silvana de
Sd
Almeida
D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001161:Arteriosclerosis / Q000188:drug therapy* / Q000235:genetics; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D002784:Cholesterol / Q000097:blood; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D010597:Pharmacogenetics; D012307:Risk Factors
D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein; D002784:Cholesterol