Tissue fibrosis is an eventual pathologic change of numerous chronic illnesses, which is characterized byresident fibroblasts differentiation into myofibroblasts during inflammation, coupled with excessiveextracellular matrix deposition in tissues, ultimately leading to failure of normal organ function. Now,there are many mechanistic insights into the pathogenesis of tissue fibrosis, which facilitate the discoveryof effective antifibrotic drugs. Moreover, many chronic diseases remain a significant clinical unmetneed. For the past five years, many research works have undoubtedly addressed the functionaldependency of ginsenosides in different types of fibrosis and the successful remission in various animalmodels treated with ginsenosides. Caveolin-1, interleukin, thrombospondin-1 (TSP-1), liver X receptors(LXRs), Nrf2, microRNA-27b, PPARd-STAT3, liver kinase B1 (LKB1)-AMPK, and TGF-b1/Smads are potentialtherapy targeting using ginsenosides. Ginsenosides can play a targeting role and suppress chronicinflammatory response, collagen deposition, and epithelialemesenchymal transition (EMT), as well asmyofibroblast activation to attenuate fibrosis. In this report, our aim was to focus on the therapeuticprospects of ginsenosides in fibrosis-related human diseases making use of results acquired from variousanimal models. These findings should provide important therapeutic clues and strategies for theexploration of new drugs for fibrosis treatment.