{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T13:22:30Z","timestamp":1787750550476,"version":"build-2784847793"},"reference-count":63,"publisher":"Ovid Technologies (Wolters Kluwer Health)","funder":[{"DOI":"10.13039\/spnnwu3rgb7s","name":"National Key Research and Development Program of China","doi-asserted-by":"publisher","award":["2019YFA0802704"],"award-info":[{"award-number":["2019YFA0802704"]}],"id":[{"id":"10.13039\/spnnwu3rgb7s","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/spvlg0gw1mon","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31771620"],"award-info":[{"award-number":["31771620"]}],"id":[{"id":"10.13039\/spvlg0gw1mon","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/spixdxqtoe1w","name":"Research Startup Fund of Southwest University","doi-asserted-by":"publisher","award":["SWU117064"],"award-info":[{"award-number":["SWU117064"]}],"id":[{"id":"10.13039\/spixdxqtoe1w","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"abstract":"\n Key Points<\/jats:title>\n \n \n \n \n Parathyroid hormone receptor 1 (Pth1r) localized to renal epithelial primary cilia and underwent parathyroid hormone\u2013induced ciliary trafficking\n via<\/jats:italic>\n a conserved valine x proline motif, independent of polycystins.\n <\/jats:p>\n <\/jats:list-item>\n \n Pth1r inactivation reduced cyst growth, epithelial proliferation, and fibrosis in both developmental and adult-onset autosomal dominant polycystic kidney disease mouse models.<\/jats:p>\n <\/jats:list-item>\n \n \n Parathyroid hormone activated cAMP signaling, primary cilia enabled efficient cAMP-responsive element-binding phosphorylation, and cinacalcet suppressed parathyroid hormone to slow cyst progression\n in vivo<\/jats:italic>\n .\n <\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n \n Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in\n PKD1<\/jats:italic>\n or\n PKD2<\/jats:italic>\n , which encode the ciliary proteins polycystin-1 and polycystin-2, respectively. Genetic ablation of primary cilia or disruption of ciliary membrane protein trafficking markedly suppresses cyst formation in adult-onset ADPKD models, indicating that cilia harbor membrane-associated signaling pathways that promote cyst progression. However, the specific ciliary receptors mediating these extracellular cyst promoting signals remain poorly defined.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We performed RiboTag-based translational profiling of early cystic kidneys in genetic mouse models of ADPKD to identify differentially expressed genes, with a focus on transmembrane protein-coding candidates. The localization and function of parathyroid hormone receptor 1 (Pth1r) were examined using immunofluorescence, genetic inactivation in developmental and adult-onset ADPKD models, and\n in vitro<\/jats:italic>\n studies of renal epithelial cells. Downstream signaling was assessed by cAMP measurements and cAMP-responsive element-binding phosphorylation analysis. Therapeutic relevance was evaluated using the calcimimetic cinacalcet.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n RiboTag profiling identified upregulation of\n Pth1r<\/jats:italic>\n in early cystic kidneys. Pth1r localized to primary cilia across nephron segments, and its genetic inactivation significantly attenuated cyst growth in both developmental and adult-onset ADPKD models.\n In vitro<\/jats:italic>\n , parathyroid hormone (PTH) promoted Pth1r trafficking to cilia through a conserved valine x proline motif independently of polycystins. PTH stimulation increased intracellular cAMP levels in renal epithelial cells, with efficient downstream activation requiring intact primary cilia.\n In vivo<\/jats:italic>\n , cAMP-responsive element-binding phosphorylation was increased during cyst progression in\n Pkd1<\/jats:italic>\n -mutant kidneys and was partially reduced by\n Pth1r<\/jats:italic>\n inactivation. Cinacalcet treatment reduced cystic burden and normalized circulating PTH levels.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n These findings support a role for Pth1r as a ciliary G protein\u2013coupled receptor linking systemic PTH signaling to cyst-promoting pathways in ADPKD.<\/jats:p>\n <\/jats:sec>","DOI":"10.1681\/asn.0000001170","type":"journal-article","created":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T11:01:17Z","timestamp":1782212477000},"update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Parathyroid Hormone Receptor 1 Facilitates Cyst Growth in Genetic Models of Autosomal Dominant Polycystic Kidney Disease"],"prefix":"10.1681","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-2740-2987","authenticated-orcid":false,"given":"Zhaohui","family":"Wu","sequence":"first","affiliation":[{"name":"Institute of Developmental Biology and Regenerative Medicine, Southwest University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-1419-5198","authenticated-orcid":false,"given":"Mengyan","family":"Sun","sequence":"additional","affiliation":[{"name":"Institute of Developmental Biology and Regenerative Medicine, Southwest University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingqiang","family":"Hu","sequence":"additional","affiliation":[{"name":"Institute of Developmental Biology and Regenerative Medicine, Southwest University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-5961-3401","authenticated-orcid":false,"given":"Qingru","family":"Yu","sequence":"additional","affiliation":[{"name":"Institute of Developmental Biology and Regenerative Medicine, Southwest University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pan","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Developmental Biology and Regenerative Medicine, Southwest University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingfei","family":"Luo","sequence":"additional","affiliation":[{"name":"Institute of Developmental Biology and Regenerative Medicine, Southwest University, Chongqing, China"},{"name":"School of Life Sciences, Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-8403-9603","authenticated-orcid":false,"given":"Ming","family":"Ma","sequence":"additional","affiliation":[{"name":"Institute of Developmental Biology and Regenerative Medicine, Southwest University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2026,6,24]]},"reference":[{"issue":"6","key":"B1-20260810","doi-asserted-by":"crossref","first-page":"881","DOI":"10.1016\/0092-8674(94)90137-6","article-title":"The polycystic kidney disease 1 gene encodes a 14 kb transcript and lies within a duplicated region on chromosome 16","volume":"77","year":"1994","journal-title":"Cell."},{"issue":"5266","key":"B2-20260810","doi-asserted-by":"crossref","first-page":"1339","DOI":"10.1126\/science.272.5266.1339","article-title":"PKD2, a gene for polycystic kidney disease that encodes an integral membrane protein","volume":"272","author":"Mochizuki","year":"1996","journal-title":"Science."},{"issue":"47","key":"B3-20260810","doi-asserted-by":"crossref","first-page":"18688","DOI":"10.1073\/pnas.0708217104","article-title":"Essential role of cleavage of polycystin-1 at G protein-coupled receptor proteolytic site for kidney tubular 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