Fig. 8.

Schematic representation of a working model. TTP modulates both inflammation and lipid metabolism. Left: During normal physiological condition, TTP acts as an anti-inflammatory molecule by degrading pro-inflammatory TNFalpha mRNA and potentially other pro-inflammatory cytokine mRNAs. Concurrently, TTP increases VLDL/LDL cholesterol indirectly by degrading negative up-regulator INSIG1 mRNA or indirectly by stabilizing HMG-CoA reductase/SREBF1 mRNAs. Right: under pathological conditions, bone marrow TTP deficiency in LDLR^−/− mice increased inflammation by stabilizing TNFalpha mRNA and potential other pro-inflammatory cytokine mRNAs and increasing mtROS production. At the same, TTP deficiency indirectly decreases VLDL/LDL cholesterol by potentially stabilizing the insulin induced gene 1 (INSIG1) mRNA or indirectly by destabilizing the mRNA of HMG‐CoA reductase or SREBF1 mRNAs. Increased inflammation, mtROS, and reduced lipids offsets each other, resulting in unchanged atherosclerosis in BM TTP deficient mice.