has anti-inflammatory effects and (in mice) induce hepatocyte proliferation via induction of microRNA let7c-signaling cascades [66, 67]. In mouse models, but not in humans, activation of PPARα induces hepatic carcinogenesis, which is in part explained by ROS production [68, 69] and induction of microRNA let7c that degrades the c-myc oncogene. Initially an orphan NR, PPARα is known to be the receptor for fibrates in diacylglycerol has been identified as an endogeneousthe therapy of hypertriglyceridemia – and recently a ligand [21], produced by the enzyme FAS, which in turn is activated by PPARα and other NRs. Emphasizing the cross-talk between NRs, FXR and LXR are known to activate PPARα signaling while VDR appears to repress PPARα signaling [58, 70, 71]. Post-transcriptionally, PPARα protein expression is repressed by microRNA 10b, which is associated with metastasis formation in a variety of cancers [72
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