Elisabetta Ceni

TL;DR: Oral administration of TZD reduced extracellular matrix deposition and HSC activation in both toxic and cholestatic models of liver fibrosis, indicating that PPARgamma activation in HSC retards fibrosis in vivo and suggest the use of TzD for the treatment of Liver fibrosis.

TL;DR: Ethanol oxidative metabolism influences intracellular signaling pathways and deranges the transcriptional control of several genes, leading to fat accumulation, fibrogenesis and activation of innate and adaptive immunity, which plays a key role in the development and progression of ALD.

TL;DR: Results indicate that neutrophil‐derived ROS may contribute to the development of hepatic fibrosis associated with alcoholic hepatitis and NO produced by neutrophils may exert a “protective” antioxidant effect by operating as a scavenger of superoxide anion.

TL;DR: The findings suggest that MMP‐2 is required for the mitogenic and proinvasive effects of ROS on HSC and demonstrate that ERK1/2 and PI3K are the main signals involved in ROS‐mediated M MP‐2 expression.

TL;DR: The results indicate that depression of PPARγ expression and activity is involved in HSC proliferation and that thePPARγ ligand‐mediated activation exerts a previously unrecognized inhibition of PDGF‐induced mitogenesis in activated human HSC.