[Hepatic stellate cells and oxidative stress].

Hepatic fibrosis is a wound-healing response that takes place during chronic liver injury and is characterized by excessive production and deposition of extracellular matrix (ECM) components, mainly collagen type I. Hepatic stellate cells (HSC) are responsible for the excessive production of scar tissue during liver fibrosis. Activation of HSC, the main step in the development of hepatic fibrosis, is mediated by cytokines and reactive oxygen species (ROS) released by damaged hepatocytes and/or activated Kupffer cells and even HSC themselves. While HSC usually remain quiescent, in response to factors promoting liver injury they undergo activation and become highly proliferative and fibrogenic. Indeed a key feature of HSC activation is uncontrolled production of collagen type I. Collagen is a heterotrimeric protein composed of two a1 chains and one a2 chain forming a triple helix structure. Initiation of HSC activation is largely due to paracrine stimulation, whereas the perpetuation of such activated state involves autocrine as well as paracrine loops. This review focuses on the role of oxidant stress on the activation of stellate cells.