{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T09:55:19Z","timestamp":1784800519161,"version":"3.55.0"},"reference-count":43,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2018,3,20]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Vascular calcification and increased cardiovascular morbidity and mortality are closely related in patients with end\u2010stage renal disease and diabetes mellitus. Specific protein 1 (Sp1) is a transactivation molecule that plays a crucial role in the regulation of apoptosis, fibrosis, angiogenesis, and other pathological disorders. There is evidence that specific protein 1 (Sp1) directly stimulates the transcription of bone morphogenetic protein 2 (\n              <jats:styled-content style=\"fixed-case\">BMP<\/jats:styled-content>\n              2) and that\n              <jats:styled-content style=\"fixed-case\">BMP<\/jats:styled-content>\n              2 plays a key role in the calcification process in the\n              <jats:styled-content style=\"fixed-case\">BMP<\/jats:styled-content>\n              2\u2013expressing F9 cell model system. Here, we investigated whether Sp1 plays an important role in vascular calcification and its potential regulatory mechanism in vascular calcification.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              In this study, vascular calcification was induced in male Wistar rats by administration of nicotine (25\u00a0mg\/kg) and vitamin D3 (300\u00a0000\u00a0IU\/kg). These rats were randomly selected for treatment with adenovirus harboring Sp1 knockdown gene or empty virus. The mechanism of Sp1 in vascular smooth muscle cells cultured in high phosphate medium was studied. Based on our findings, the Sp1 gene silencing or inhibition improved calcium deposition, which was partly achieved by inhibiting phenotype switch, apoptosis, and matrix vesicle release of vascular smooth muscle cells. Moreover, Sp1 can activate\n              <jats:styled-content style=\"fixed-case\">BMP<\/jats:styled-content>\n              2 transcription by binding to the Sp1\u2010binding element of the\n              <jats:styled-content style=\"fixed-case\">BMP<\/jats:styled-content>\n              2 promoter.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Overall, elevated Sp1 exerts a pro\u2010apoptotic effect, promoting\n              <jats:styled-content style=\"fixed-case\">BMP<\/jats:styled-content>\n              2 transcription and further accumulating vascular calcification. Proper and timely regulation of Sp1 expression may be a potential strategy for treatment of aging, end\u2010stage renal disease, and diabetic\u2010related macrovascular disease treatment.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.117.007555","type":"journal-article","created":{"date-parts":[[2018,3,23]],"date-time":"2018-03-23T09:30:18Z","timestamp":1521797418000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":39,"title":["Sp1 Plays an Important Role in Vascular Calcification Both In Vivo and In Vitro"],"prefix":"10.1161","volume":"7","author":[{"given":"Xinyu","family":"Zhang","sequence":"first","affiliation":[{"name":"Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, the State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, Shandong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Li","sequence":"additional","affiliation":[{"name":"Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, the State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, Shandong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoteng","family":"Qin","sequence":"additional","affiliation":[{"name":"Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, the State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, Shandong, 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