Objective To analyze the cell-cell communication and molecular characteristics of intrauterine adhesion tissues, and further investigate the immune microenvironment and cellular interactions. Methods Three patients with moderate IUA who underwent hysteroscopic surgery at Tangdu Hospital, Air Force Medical University, from February 2025 to June 2025 were enrolled as the IUA group. Normal women who underwent hysteroscopy during the proliferative phase (within 3-7 days after menstruation) of the matched period were selected as the control group. Endometrial tissue samples were collected intraoperatively, and immunofluorescence staining was performed to validate the key findings. Single-cell transcriptomic data from public databases were integrated and experimentally validated using the clinical samples. Results Under the pathological state of IUA, the overall number of intercellular communications within the tissue remained basically comparable to that of the control group. However, compared with the control group, the overall interaction strength in the IUA group decreased from 204.857 to 159.238, suggesting the potential presence of widespread cellular communication barriers and molecular network dysfunction in the IUA endometrium. Analysis of intercellular communication signals revealed that, compared to the control endometrial tissues, the overall strength of signaling pathways initiated or received by M1 macrophages (CD86+) was significantly increased in the IUA samples, indicating that this cell subpopulation plays an active role in inflammatory regulation within the IUA microenvironment. The infiltration proportion of F4/80+CD86+ (M1) macrophages in the endometrial tissues of the IUA group was significantly higher than that of the control group, and the difference was statistically significant (P<0.05). Further analysis demonstrated that Pro-inflammatory macrophages link endothelial and stromal cells via the TGF-β and IL-1 signaling pathways to synergistically drive endometrial fibrosis. Conclusion This study systematically reveals the critical role of pro-inflammatory macrophages and their mediated TGF-β and IL-1 signaling pathways in IUA, providing a foundation for understanding the pathogenesis of IUA and developing targeted therapies