{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T19:33:57Z","timestamp":1790883237759,"version":"4.1.0"},"reference-count":36,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,11]]},"abstract":"\n Background<\/jats:title>\n \n Hyperphosphatemia is a major factor promoting the formation of arterial medial calcification in chronic kidney disease (\n CKD<\/jats:styled-content>\n ). However, arterial medial calcification begins to occur during the early stages of\n CKD<\/jats:styled-content>\n , when hyperphosphatemia is not yet apparent. It is predicted that other factors also play a role. The aim of the present study was to determine the role of pro\u2010inflammatory nuclear factor\u2010\u03baB (\n NF<\/jats:styled-content>\n \u2010\u03baB) signaling in smooth muscle cells (\n SMC<\/jats:styled-content>\n s) for phosphate\u2010induced arterial medial calcification in\n CKD<\/jats:styled-content>\n mice.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n We first sought to establish a novel mouse model of\n CKD<\/jats:styled-content>\n with arterial medial calcification.\n CKD<\/jats:styled-content>\n was induced in\n DBA<\/jats:styled-content>\n \/2 mice by feeding them a low concentration of adenine, and these mice were fed a normal or high\u2010phosphorus diet. Severe calcification was seen in\n CKD<\/jats:styled-content>\n mice fed the high\u2010phosphorus diet, while it was undetectable in\n CKD<\/jats:styled-content>\n mice fed the normal phosphorus diet or control mice fed the high\u2010phosphorus diet. Arterial medial calcification was accompanied by phenotypic switching of\n SMC<\/jats:styled-content>\n s into osteogenic cells. Interestingly,\n NF<\/jats:styled-content>\n \u2010\u03baB inhibitors, tempol and triptolide, both reduced arterial medial calcification in\n CKD<\/jats:styled-content>\n mice fed the high\u2010phosphorus diet. Moreover, formation of arterial medial calcification, as well as\n SMC<\/jats:styled-content>\n phenotypic switching, was also markedly attenuated in transgenic mice, in which the\n NF<\/jats:styled-content>\n \u2010\u03baB activity was inhibited selectively in\n SMC<\/jats:styled-content>\n s. Mechanistic studies revealed that Kr\u00fcppel\u2010like factor 4 was involved in\n NF<\/jats:styled-content>\n \u2010\u03baB\u2010induced\n SMC<\/jats:styled-content>\n phenotypic switching and calcification.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Results of the present studies suggest that the\n NF<\/jats:styled-content>\n \u2010\u03baB signaling in\n SMC<\/jats:styled-content>\n s plays an important role in high phosphate\u2010induced arterial medial calcification in\n CKD<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.117.007248","type":"journal-article","created":{"date-parts":[[2017,11,17]],"date-time":"2017-11-17T01:10:35Z","timestamp":1510881035000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":55,"title":["Smooth Muscle\u2013Selective Nuclear Factor\u2010\u03baB Inhibition Reduces Phosphate\u2010Induced Arterial Medial Calcification in Mice With Chronic Kidney Disease"],"prefix":"10.1161","volume":"6","author":[{"given":"Tadashi","family":"Yoshida","sequence":"first","affiliation":[{"name":"Apheresis and Dialysis Center, School of Medicine, Keio University, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maho","family":"Yamashita","sequence":"additional","affiliation":[{"name":"Apheresis and Dialysis Center, School of Medicine, Keio University, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chihiro","family":"Horimai","sequence":"additional","affiliation":[{"name":"Apheresis and Dialysis Center, School of Medicine, Keio University, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matsuhiko","family":"Hayashi","sequence":"additional","affiliation":[{"name":"Apheresis and Dialysis Center, School of Medicine, Keio University, Tokyo, 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