The biological processes that are influenced by hepatic stellate cells are indicated in blue. At early phases of liver regeneration, hepatic stellate cells promote the proliferation of liver progenitor cells and hepatocytes. They also stimulate angiogenesis in the wounded area and assist in the recruitment of hematopoietic stem cells and immune cells to the liver (reviewed in ref. 48). Recent studies suggest that activated hepatic stellate cells may undergo a mesenchymal-to-epithelial transition to transdifferentiate into liver progenitor cells. At late phases, hepatic stellate cells participate in the termination of regeneration, likely via high expression of TGF-β. Hepatic stellate cells have also been proposed to contribute to HCC development, potentially through dysregulation of some aspects of liver regeneration described above. On the other hand, liver fibrosis, which results from ectopic hepatic stellate cell activation, has controversial roles in HCC. Most evidence suggests that fibrosis promotes HCC, but it is possible that in some clinical settings fibrosis and HCC might occur due to the same underlying factor(s) rather than one promoting the other.