Pterygium is a prevalent ocular disorder characterized by the proliferation of fibrovascular tissue beneath the conjunctiva. The precise role of monocyte chemotactic protein-induced protein 1 (MCPIP1) in the pterygium remains elusive.Immunohistochemistry, Western blot, and quantitative RT-PCR were used to analyze the expression of MCPIP1 and other regulators. The role of MCPIP1 in pterygium fibrosis was assessed both in vitro and in vivo. Further, Co-immunoprecipitation and ubiquitination assays were performed to investigate the impact of MCPIP1 on the TRAF6-BECN1 signaling pathway. The role of MCPIP1 in autophagy regulation was studied through immunofluorescence experiments, while transwell migration and wound-healing assays were employed to assess the migratory and proliferative capabilities of human pterygium fibroblast (HPF) cells. Additionally, in vitro transcription and uridylylation experiments provided mechanistic insights into the regulatory role of terminal uridyltransferase 7 (TUT7) on MCPIP1 mRNA.The results showed that MCPIP1 negatively regulates the fibrosis and autophagy of HPF cells, thereby inhibiting the development of pterygium. In terms of its mechanism, MCPIP1 facilitated the assembly of the TRAF6-BECN1 complex, augmented BECN1 ubiquitination, induced autophagy, and attenuated cell migration and proliferation abilities while suppressing HPFs' cell fibrosis. The function of MCPIP1 was weakened by TUT7, which reduced the stability of MCPIP1 mRNA and thus alleviated the negative regulatory effect of MCPIP1 on pterygium.In summary, the current study revealed that MCPIP1 promotes autophagy by positively regulating the TRAF6-BECN1 signaling pathway, thereby suppressing pterygium development. Conversely, TUT7 uridylylation modulated MCPIP1's regulation of pterygium.