G-Protein-Coupled Receptor CXCR7 Is Overexpressed in Human and Murine Endometriosis

Nicola Pluchino, Ramanaiah Mamillapalli, Irene Moridi, Moridi I, Reshef Tal, Hugh S. Taylor
Reproductive sciences (Thousand Oaks, Calif.) · 2018 · vol. 25(8) , pp. 1168–1174 · doi:10.1177/1933719118766256 · PMID:29587613 · PMC6346303 · W2795313790
article OA: closed CC0 ⤵ 14 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

This study investigated the presence of G-protein-coupled receptor CXCR7 and found it to be overexpressed in both human and murine endometriosis.

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Abstract

Endometriosis is a chronic inflammatory disease. Dysfunctional regulation of chemokines and chemokine receptors is a crucial aspect of endometriosis pathogenesis. Chemokine G-protein-coupled receptors (GPCRs) are important drug targets that regulate inflammation and immunity. Recently, CXCR7, a C-X-C motif containing GPCR, has been identified as a receptor for chemokine ligand CXCL12, one of the best characterized chemokines for cell trafficking, angiogenesis, and cell proliferation in cancer and inflammation. Here, we investigated the expression and localization of CXCR7 in human endometriosis and a murine model of the disease. Normal endometrial epithelium and stroma showed undetectable or very low expression of CXCR7, without any significant changes across phases of the menstrual cycle in humans. CXCR7 is significantly upregulated in endometriosis, showing higher staining in glands and in associated vessels. The mouse model recapitulated the human findings. In conclusion, overexpression of CXCR7 in different cellular populations of endometriosis microenvironment may play a role in the pathogenesis and represent a novel target for treatment.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Receptors, CXCR Animals Disease Models, Animal Endometriosis Endometrium Epithelial Cells Epithelial Cells Female Humans Mice, Inbred C57BL Receptors, CXCR Stromal Cells Stromal Cells

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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Cited by (14)

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