Liver fibrosis represents a pathological reparative process for the liver that occurs due to persistent harm, closely linked to sustained liver damage and inflammation. In healthy livers, hepatic stellate cells remain quiescent; however, following liver injury, their transformation into myofibroblasts results in extracellular matrix deposition, thereby worsening the developing stages of hepatic fibrosis. According to research, the main cause of liver fibrosis is the activation of hepatic stellate cells. Significant progress has been made in the study of the development and regression mechanisms of liver fibrosis in recent years, as well as a better understanding of the function of hepatic stellate cells in the fibrous process. The metabolic reprogramming of hepatic stellate cells is a crucial factor facilitating their activation and is essential for their effector roles and anabolic requirements; current research indicates that mechanosignaling is a significant regulator of cellular metabolism. This study summarizes the impact of hepatic stellate cell energy metabolism on fibrosis progression, examines the relationship between mechanomechanics and cellular metabolism, and discusses the therapeutic possibility of targeting cellular energy metabolism.