ArticleEuropean journal of histochemistry : EJH2024
CCL18 promotes endometriosis by increasing endometrial cell migration and neuroangiogenesis.
Article in European journal of histochemistry : EJH, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Superficial Peritoneal Endometriosis Beyond Surgical Diagnosis: A Narrative Review of Emerging Functional and Molecular Perspectives.Medicina (Kaunas, Lithuania) · 2026Review
- Targeting EphA2 suppresses the proliferation, migration and invasion of endometriosisEuropean journal of histochemistry : EJH · 2025Article
- Causal analysis of dietary preferences and the risk of endometriosis using large-scale population data.Scientific reports · 2025Article
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8 authors.
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Abstract
Endometriosis is an estrogen-dependent inflammatory gynecological disease whose pathogenesis is unclear. C-C motif chemokine ligand 18 (CCL18), a chemokine, is involved in several inflammatory diseases. In this study, we aimed to investigate the role of CCL18 in endometriosis and its underlying mechanisms. Human endometrium and peritoneal fluid were obtained from women with and without endometriosis for molecular studies. The expression level of CCL18 in each tissue sample was examined by RNA sequencing analysis, quantitative PCR analysis and immunohistochemistry staining. The effects of CCL18 on cell migration, tube formation and neurite growth were investigated in vitro using primary endometrial cells, human umbilical vein endothelial cells (HUVECs) and dorsal root ganglion (DRG) neurons, respectively. Moreover, the development of endometriosis in mice was studied in vivo by blocking CCL18. CCL18 was shown to be overexpressed in endometrial foci and peritoneal fluid in women with endometriosis and was positively correlated with endometriosis pain. In vitro, CCL18 promoted the migration of ectopic endometrial cells, tube formation of HUVECs, and nerve outgrowth of DRG neurons. More importantly, inhibition of CCL18 significantly suppressed lesion development, angiogenesis, and nerve infiltration in a mouse model of endometriosis. In conclusion, CCL18 may play a role in the progression of endometriosis by increasing endometrial cell migration and promoting neuroangiogenesis.
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