Casein Kinase 1α Agonist Pyrvinium Promotes Autophagy to Suppress Endometriosis in Mice

Endometriosis is a prevalent gynecological disorder characterized by the ectopic presence of endometrial tissue and chronic inflammation. This study aimed to explore the therapeutic potential of the Casein kinase 1 alpha (CK1α) agonist pyrvinium in endometriosis. Human endometrial stromal cells and an in vivo mouse model of endometriosis were employed. Quantitative PCR was used to assess the mRNA levels of CK1α and autophagy-related genes, while Western blot analysis measured their protein expression. Immunohistochemical staining was performed to detect CK1α and Atg7 in ectopic lesion tissues. Additionally, enzyme-linked immunosorbent assay quantified inflammatory cytokine secretion in the culture supernatants and mouse peritoneal fluid. In human endometrial stromal cells, pyrvinium treatment significantly upregulated CK1α and autophagy-related proteins and suppressed inflammatory cytokine secretion under hypoxic conditions. In the in vivo endometriosis model, pyrvinium inhibited the growth of endometriotic lesions and reduced pro-inflammatory cytokine levels. These findings suggest that pyrvinium activates CK1α, induces autophagy, and mitigates inflammatory responses in endometriosis.