Chronic liver injury results in hepatic fibrosis, which is characterized by extensive deposition of extracellular matrix proteins mainly produced by fibrogenic myofibroblasts (MFs) which are not present in the normal liver. Hepatic MFs are a heterogeneous population which is mainly composed of activated hepatic stellate cells (aHSCs), portal fibroblasts (aPFs) and bone marrow-derived circulating fibrocytes, and/or mesenchymal stem cells. While the contribution of aHSCs and aPFs to liver-resident MFs is well documented, the role of fibrocytes in pathogenesis of liver fibrosis is still controversial. It remains unknown if fibrocytes serve as a significant source of MFs or mainly mediate pro-fibrogenic signals to the neighboring cells in response to chronic liver injury. The current review will summarize the up-to-date understanding of the fibrocyte functions, and discuss the similarities and differences of fibrocyte activation in liver and other parenchymal organs. Specifically, here we provide an overview on (1) the role of cytokines and growth factors in recruitment of fibrocytes to the damaged organ; (2) the role of circulating fibrocytes as possible biomarker of fibrogenic diseases; and (3) the role of human Serum amyloid P in pharmacological inhibition of fibrocyte and macrophage recruitment to fibrosing organs as a potential novel strategy for anti-fibrotic therapy.