Transforming growth factor‑β1 reduces apoptosis via autophagy activation in hepatic stellate cells.

Autophagy is a metabolic process that is important in fibrogenesis, in which cellular components are degraded by lysosomal machinery. Transforming growth factor β1 (TGF‑β1) is a potent fibrogenic cytokine involved in liver fibrosis; however, it remains elusive whether autophagy is regulated by TGF‑β1 in this process. In the present study, the function of TGF‑β1‑mediated autophagy in the proliferation and apoptosis of hepatic stellate cells (HSCs) was investigated.

β-Nerve growth factor attenuates hepatocyte injury induced by D-galactosamine in vitro via TrkA NGFR.

Nerve growth factor (NGF) regulates the proliferation, differentiation and survival of cells and is also involved in the wound healing and tissue remodeling processes. The biological effects of NGF are dependent upon receptor signal-mediating functions, which differ between cells. This study attempted to investigate the hepatoprotective effect and possible mechanism of β-NGF on D-galactosamine (D-GalN)-injured human liver L-02 cell lines.