Description
Hepatic fibrosis represents the final common pathway for many types of chronic liver disease. The hepatic stellate cell (HSC) is important in liver fibrogenesis. Hepatic stellate cells play a central role in matrix turnover by synthesising matrix and regulating its degradation through expression of tissue inhibitors of metalloproteinase (TIMPs). Spontaneous resolution from relatively advanced liver fibrosis is possible. Key features of recovery are apoptosis of HSC, a decreased expression of TIMPs 1 and 2 and an increase in collagenase activity. A failure of matrix degradation and a failure of HSC apoptosis may significantly contribute to the progression of fibrosis. Greater understanding of the mechanisms that promote recovery compared to progression of fibrosis may hold the key to future therapeutic developments.
