circPTPN12/miR-21-5 p/ΔNp63α pathway contributes to human endometrial fibrosis

Emerging evidence demonstrates the important role of circular RNAs (circRNAs) in regulating pathological processes in various diseases including organ fibrosis. Endometrium fibrosis is the leading cause of uterine infertility, but the role of circRNAs in its pathogenesis is largely unknown. Here, we provide the evidence that upregulation of circPTPN12 in endometrial epithelial cells (EECs) of fibrotic endometrium functions as endogenous sponge of miR-21-5 p to inhibit miR-21-5 p expression and activity, which in turn results in upregulation of Delta Np63 alpha to induce the epithelial mesenchymal transition (EMT) of EECs (EEC-EMT). In a mouse model of endometrium fibrosis, circPTPN12 appears to be a cofactor of driving EEC-EMT and administration of miR-21-5 p could reverse this process and improve endometrial fibrosis. Our findings revealed that the dysfunction of circPTPN12/miR-21-5 p/Delta Np63 alpha pathway contributed to the pathogenesis of endometrial fibrosis.

Automated summary

Emerging evidence suggests a crucial role of circRNAs in regulating pathological processes, with circPTPN12 identified as a factor in endometrial fibrosis pathology. Dysfunction of the circPTPN12 pathway contributes to the pathogenesis of endometrial fibrosis.