{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T20:49:09Z","timestamp":1786135749481,"version":"build-2736575974"},"reference-count":67,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","funder":[{"DOI":"10.13039\/501100000780","name":"European Commission","doi-asserted-by":"publisher","award":["FP7-264663"],"award-info":[{"award-number":["FP7-264663"]}],"id":[{"id":"10.13039\/501100000780","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002428","name":"Austrian Science Fund","doi-asserted-by":"publisher","award":["P-29948-B28"],"award-info":[{"award-number":["P-29948-B28"]}],"id":[{"id":"10.13039\/501100002428","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002428","name":"Austrian Science Fund","doi-asserted-by":"publisher","award":["P-32840-B"],"award-info":[{"award-number":["P-32840-B"]}],"id":[{"id":"10.13039\/501100002428","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK12165601"],"award-info":[{"award-number":["R01DK12165601"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK122259"],"award-info":[{"award-number":["R01DK122259"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007496","name":"Biomedical Laboratory Research and Development, VA Office of Research and Development","doi-asserted-by":"publisher","award":["I01BX005851"],"award-info":[{"award-number":["I01BX005851"]}],"id":[{"id":"10.13039\/100007496","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007496","name":"Biomedical Laboratory Research and Development, VA Office of Research and Development","doi-asserted-by":"publisher","award":["1IK6BX004835"],"award-info":[{"award-number":["1IK6BX004835"]}],"id":[{"id":"10.13039\/100007496","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2022,7]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Impaired mineral ion metabolism is a hallmark of CKD\u2013metabolic bone disorder. It can lead to pathologic vascular calcification and is associated with an increased risk of cardiovascular mortality. Loss of calcium-sensing receptor (CaSR) expression in vascular smooth muscle cells exacerbates vascular calcification\n                      <jats:italic toggle=\"yes\">in vitro.<\/jats:italic>\n                      Conversely, vascular calcification can be reduced by calcimimetics, which function as allosteric activators of CaSR.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To determine the role of the CaSR in vascular calcification, we characterized mice with targeted\n                      <jats:italic toggle=\"yes\">Casr<\/jats:italic>\n                      gene knockout in vascular smooth muscle cells (\n                      <jats:italic toggle=\"yes\">SM22\u03b1<\/jats:italic>\n                      CaSR\n                      <jats:italic toggle=\"yes\">\u0394flox\/\u0394flox<\/jats:italic>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Vascular smooth muscle cells cultured from the knockout (KO) mice calcified more readily than those from control (wild-type) mice\n                      <jats:italic toggle=\"yes\">in vitro.<\/jats:italic>\n                      However, mice did not show ectopic calcifications\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      but they did display a profound mineral ion imbalance. Specifically, KO mice exhibited hypercalcemia, hypercalciuria, hyperphosphaturia, and osteopenia, with elevated circulating fibroblast growth factor 23 (FGF23), calcitriol (1,25-D\n                      <jats:sub>3<\/jats:sub>\n                      ), and parathyroid hormone levels. Renal tubular\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      -Klotho protein expression was increased in KO mice but vascular\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      -Klotho protein expression was not. Altered CaSR expression in the kidney or the parathyroid glands could not account for the observed phenotype of the KO mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These results suggest that, in addition to CaSR\u2019s established role in the parathyroid-kidney-bone axis, expression of CaSR in vascular smooth muscle cells directly contributes to total body mineral ion homeostasis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2021040585","type":"journal-article","created":{"date-parts":[[2022,5,23]],"date-time":"2022-05-23T12:17:01Z","timestamp":1653308221000},"page":"1323-1340","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":16,"title":["Impaired Mineral Ion Metabolism in a Mouse Model of Targeted Calcium-Sensing Receptor (CaSR) Deletion from Vascular Smooth Muscle Cells"],"prefix":"10.1681","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7017-5426","authenticated-orcid":false,"given":"Martin","family":"Schepelmann","sequence":"first","affiliation":[{"name":"School of Biosciences, Cardiff University, Cardiff, United Kingdom"},{"name":"Institute of Pathophysiology and Allergy Research, Medical University of Vienna, Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3118-5813","authenticated-orcid":false,"given":"Marianna","family":"Ranieri","sequence":"additional","affiliation":[{"name":"Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irene","family":"Lopez-Fernandez","sequence":"additional","affiliation":[{"name":"School of Biosciences, Cardiff University, Cardiff, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6689-2131","authenticated-orcid":false,"given":"Thomas S.","family":"Webberley","sequence":"additional","affiliation":[{"name":"School of Biosciences, Cardiff University, Cardiff, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8719-4367","authenticated-orcid":false,"given":"Sarah C.","family":"Brennan","sequence":"additional","affiliation":[{"name":"School of Biosciences, Cardiff University, Cardiff, United Kingdom"},{"name":"Charles Perkins Centre, University of Sydney, Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7534-7995","authenticated-orcid":false,"given":"Polina L.","family":"Yarova","sequence":"additional","affiliation":[{"name":"School of Biosciences, Cardiff University, Cardiff, United Kingdom"},{"name":"Translational and Clinical Research 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