Background: Liver fibrosis is a diffuse excessive deposition of extracellular matrix (especially collagen) in the liver. It is a repair response of the body to chronic liver injury. AIM2 regulates the activation of caspase-1 and thus promotes the maturation and secretion of the cytokine precursors of pro-IL-1β and pro-IL-18. It also regulates caspase-1-dependent pyroptosis. However, it is unclear whether AIM2 is involved in the pathogenesis of liver fibrosis. Methods: In the present study, CCK-8 was used to measure cell viability. Evaluation of functional AIM2-induced ECM and fibrosis using protein blotting and quantitative real-time polymerase chain reaction. Validation of the effect of the AIM2/ASC/caspase-1 signalling axis on liver fibrosis using ASC siRNA and caspase-1 inhibitors. Overexpression of AIM2 in cells using transient techniques to evaluate the extent of collagen and focal death. Cells with COL1A1 (pGL3-COL1A1) were constructed and characterised. Activation of its activity by AIM2 was measured in vitro. 2 Results: Absent in melanoma 2 (AIM2) is a pro-inflammatory cytokine that plays a key role in inflammation. However, the role of hepatocytes in AIM2 expression remains unclear. In the present study, we demonstrate that AIM2 increases COL1A1 expression via the COL1A1 promoter. AIM2 increases COL1A1 expression in a dose-dependent manner. Furthermore, we demonstrated that AIM2 failed to cause an increase in COL1A1 expression after inhibition of ASC and caspase-1 expression in HepG2 cells. These results suggest that the AIM2/ASC/caspase-1 signalling axis can induce liver fibrosis in HepG2 cells. Conclusion: Collagen I is expressed by hepatocytes through activation AIM2/ASC/caspase-1 pathway.