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

Zhou A, Aixiu Zhou, Qiongyi Cai, Cai Q, Yating Hong, Hong Y, Yuchun Lv
Journal of biochemical and molecular toxicology · 2025 · vol. 39(10) , pp. e70506 · doi:10.1002/jbt.70506 · PMID:40976863 · W4414402757
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Pyrvinium, a Casein Kinase 1α agonist, was found to suppress endometriosis in mice by promoting autophagy and reducing inflammatory cytokine secretion in both cell models and an in vivo mouse model.

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This study investigated the therapeutic potential of pyrvinium, a Casein Kinase 1α agonist, in treating endometriosis using human endometrial stromal cells and an in vivo mouse model. The researchers found that pyrvinium treatment significantly upregulated CK1α and autophagy-related proteins while suppressing inflammatory cytokine secretion under hypoxic conditions in vitro. In the animal model, pyrvinium inhibited the growth of endometriotic lesions and reduced pro-inflammatory cytokine levels in peritoneal fluid, indicating that the compound mitigates inflammation by inducing autophagy. This paper is centrally about endometriosis — specifically examining how pyrvinium promotes autophagy to suppress lesion growth and inflammation in a murine model.

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Abstract

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.
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Casein Kinase 1α Agonist Pyrvinium Promotes Autophagy to Suppress Endometriosis in Mice ABSTRACT 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. Conflicts of Interest The authors declare no conflicts of interest. Data Availability Statement Data are available upon reasonable request by contacting the corresponding author.

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Condition tags

endometriosis

MeSH descriptors

Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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