{"paper_id":"426d08ad-6ea7-4526-af1e-4c41b2692845","body_text":"There are very few treatment options for people with endometriosis, an inflammatory condition that causes pelvic pain and can be debilitating. In a new study, researchers sequenced DNA from 32 families with a history of endometriosis. They identified a genetic linkage signal on chromosome 7p13–15. There was also overrepresentation of deleterious coding variants in NPSR1 (which encodes neuropeptide S receptor 1) in people with endometriosis. These findings were replicated in a cohort of rhesus macaques with spontaneous endometriosis. Further work in a cohort of people with or without endometriosis revealed that variant rs142885915 was associated with stage III or IV endometriosis. NPSR1 was found to be expressed in glandular epithelium from eutopic and ectopic endometrium. In addition, mouse models of peritoneal inflammation or endometriosis were treated with an inhibitor of NPSR1, which reduced peritoneal inflammation and pelvic pain. The authors suggest that the NPSR1 system could be a nonhormonal target for treating endometriosis.\nThis is a preview of subscription content, access via your institution\nAccess options\nAccess Nature and 54 other Nature Portfolio journals\nGet Nature+, our best-value online-access subscription\n27,99 € / 30 days\ncancel any time\nSubscribe to this journal\nReceive 12 print issues and online access\n176,64 € per year\nonly 14,72 € per issue\nBuy this article\n- Purchase on SpringerLink\n- Instant access to the full article PDF.\n39,95 €\nPrices may be subject to local taxes which are calculated during checkout\nReferences\nOriginal article\nTapmeier, T. T. et al. Neuropeptide S receptor 1 is a nonhormonal treatment target in endometriosis. Sci. Transl Med. 13, eabd6469 (2021)\nAuthor information\nAuthors and Affiliations\nCorresponding author\nRights and permissions\nAbout this article\nCite this article\nGreenhill, C. New treatment target for endometriosis. Nat Rev Endocrinol 17, 639 (2021). https://doi.org/10.1038/s41574-021-00564-4\nPublished:\nVersion of record:\nIssue date:\nDOI: https://doi.org/10.1038/s41574-021-00564-4","source_license":"CC0","license_restricted":false}