Nuclear Receptor Nurr1 deactivate HSC through suppressing EMT

Epithelial-mesenchymal transition (EMT) plays a pivotal role in the pathogenesis of liver fibrosis, with hepatic stellate cells (HSCs) being capable of undergoing EMT. Our previous findings demonstrated that the overexpression of the nuclear receptor Nurr1 inhibited liver fibrosis.

However, the underlying mechanism remains unclear. Notably, transfection with a Nurr1-overexpressing plasmid resulted in reduced α-SMA expression and elevated E-CAD expression in HSC-T6 cells, while silencing Nurr1 had the opposite effect. Furthermore, downregulation of Nurr1 led to increased mRNA levels of α-SMA and EMT-related genes, such as Snail, Slug, and Smad3, whereas overexpression of Nurr1 had the opposite effect.