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This editorial reviews the recent evidence showing that Mallory-Denk bodies(MDBs)form in hepatocytes as the result of a drug-induced shift from the 26s proteasome formation to the immunoproteasome formation.The shift is the result of changes in gene expression induced in promoter activation,which is induced by the IFNγ and TNFa signaling pathway.This activates TLR 2 and 4 receptors.The TLR signaling pathway stimulates both the induction of a cytokine proinflammatory response and an up regulation of growth factors.The MDB-forming hepatocytes proliferate as a result of the increase in growth factor expression by the MDBforming cells,which selectively proliferate in response to drug toxicity.All of these mechanisms are induced by drug toxicity,and are prevented by feeding the methyl donors SAMe and betaine,supporting the epigenetic response of MDB formation.
This editorial reviews the recent evidence that that Mallory-Denk bodies (MDBs) form in hepatocytes as the result of a drug-induced shift from the 26s proteasome formation to the immunoproteasome formation. Shift is the result of changes in gene expression induced in promoter activation, which is induced by the IFNγ and TNFa signaling pathway. This activates TLR 2 and 4 receptors. TLR signaling pathway stimulates both the induction of a cytokine proinflammatory response and an upregulation of growth factors. The MDB-forming hepatocytes proliferate as a result of the increase in growth factor expression by the MDBforming cells, which selectively proliferate in response to drug toxicity. All of these mechanisms are induced by drug toxicity, and prevented by feeding the methyl donors SAMe and betaine, supporting the epigenetic response of MDB formation.