Hepatic fibrosis is a common disease caused by wound-healing response to a variety of chronic liver injuries; it is characterized by the imbalance of extracellular matrix synthesis and degradation. Angiotensin Ⅱ is the major effector of the renin-angiotensin system. Increasing evidence has demonstrated that the interaction of angiotensin Ⅱ with angiotensin receptor 1 plays an important role in the long-term liver injury-induced liver fibrosis by inducing the activation,proliferation and constriction of hepatic stellate cells, generation of the reactive oxygen species from activated hepatic stellate cells, and the synthesis and accumulation of collagen. In this article we focused on the role of angiotensin Ⅱ and its receptor 1 in the pathogenesis, development and therapy of liver fibrosis in recent years.