FOS expression in blood as a LDL-independent marker of statin treatment



      The expression of FOS, a gene critical for monocyte and macrophage function, can be inhibited by statins through the disruption of a cholesterol-independent signaling pathway. In this pilot study, we hypothesized that blood FOS mRNA levels will be sensitive to statin treatment independent of LDL cholesterol levels.


      Three cohorts at increased risk of or with cardiovascular disease (CVD) were studied. Blood FOS mRNA levels were measured before and after statin treatment or in patients under stable treatment.


      Statin treatment for three months significantly reduced blood FOS mRNA and LDL cholesterol levels. However, in subjects with similar LDL levels achieved by different doses of long term statin treatment, there was an inverse relationship between statin dose and FOS expression.


      FOS mRNA levels appear to be a sensitive marker of statin treatment that is dissociated from cholesterol levels.


      CAD (coronary artery disease), CVD (cardiovascular diseases), FOS (Finkel–Biskis–Jinkins osteosarcoma gene), HMG CoA reductase (3-hydroxy-3-methylglutaryl coenzyme A reductase), hsCRP (high sensitivity C-reactive protein), statin (HMG CoA reductase inhibitor)


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