Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease characterized by autoimmune-mediated destruction of intrahepatic bile ducts. Emerging evidence suggests that circular RNAs (circRNAs) play regulatory roles in autoimmune diseases, but their involvement in PBC remains unclear. This study focused on the hsa_circ_0000711 and its potential mechanism in PBC pathogenesis. The study included 46 PBC patients, 40 healthy controls, and 40 patients with other liver diseases. Human intrahepatic biliary epithelial cells (HiBEpic) were treated with 1 mM glycochenodeoxycholic acid (GCDCA) to establish a PBC cell model. Hsa_circ_0000711 was overexpressed or knocked down using plasmid transfection and siRNA, respectively. Expression levels were analysed by qPCR/Western blot, cell viability by CCK-8, and hsa_circ_0000711-miR-185-5p interaction by luciferase assay. Serum hsa_circ_0000711 levels were significantly higher in PBC patients compared to healthy controls and other liver disease groups (p < 0.0001). GCDCA-treated HiBEpic cells showed increased expression of the E2 subunit of the pyruvate dehydrogenase complex (PDC-E2) and nuclear factor of activated T cells 3 (NFATc3), along with decreased cell viability. Overexpression of hsa_circ_0000711 increased PDC-E2 and NFATc3 expression and worsened cellular injury, while its knockdown reversed these effects. The dual luciferase assay confirmed that hsa_circ_0000711 directly binds to miR-185-5p, suppressing its activity and thereby relieving the repression of NFATc3. Hsa_circ_0000711 promotes PBC progression by sponging miR-185-5p and upregulating NFATc3, leading to bile duct epithelial cell injury. These findings highlight its potential as a novel diagnostic biomarker and therapeutic target for PBC.