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However, the precise mechanisms and its contribution to cardiovascular protection remain unclear. There are currently 2 leading hypotheses: first, magnesium may bind phosphate and delay calcium phosphate crystal growth in the circulation, thereby passively interfering with calcium phosphate deposition in the vessel wall. Second, magnesium may regulate vascular smooth muscle cell transdifferentiation toward an osteogenic phenotype by active cellular modulation of factors associated with calcification. Here, the data supporting these major hypotheses are reviewed. The literature supports both a passive inorganic phosphate\u2013buffering role reducing hydroxyapatite formation and an active cell-mediated role, directly targeting vascular smooth muscle transdifferentiation. However, current evidence relies on basic experimental designs that are often insufficient to delineate the underlying mechanisms. The field requires more advanced experimental design, including determination of intracellular magnesium concentrations and the identification of the molecular players that regulate magnesium concentrations in vascular smooth muscle cells.<\/jats:p>","DOI":"10.1161\/atvbaha.117.309182","type":"journal-article","created":{"date-parts":[[2017,6,30]],"date-time":"2017-06-30T01:10:26Z","timestamp":1498785026000},"page":"1431-1445","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":117,"title":["Magnesium Counteracts Vascular Calcification"],"prefix":"10.1161","volume":"37","author":[{"given":"Anique D.","family":"ter Braake","sequence":"first","affiliation":[{"name":"From the Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands (A.D.t.B., J.H.F.d.B.); Cardiovascular Division, BHF Centre of Research Excellence, James Black Centre, King\u2019s College, London, United Kingdom (C.M.S.); and Department of Physiology, Anatomy and Genetics, University of Oxford, United Kingdom (J.H.F.d.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine M.","family":"Shanahan","sequence":"additional","affiliation":[{"name":"From the Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands (A.D.t.B., J.H.F.d.B.); Cardiovascular Division, BHF Centre of Research Excellence, James Black Centre, King\u2019s College, London, United Kingdom (C.M.S.); and Department of Physiology, Anatomy and Genetics, University of Oxford, United Kingdom (J.H.F.d.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeroen H.F.","family":"de Baaij","sequence":"additional","affiliation":[{"name":"From the Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands (A.D.t.B., J.H.F.d.B.); Cardiovascular Division, BHF Centre of Research Excellence, James Black Centre, King\u2019s College, London, United Kingdom (C.M.S.); and Department of Physiology, Anatomy and Genetics, University of Oxford, United Kingdom (J.H.F.d.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_5_2_2","first-page":"239","article-title":"Cardiovascular disease and mortality in ESRD.","volume":"11","author":"Foley RN","year":"1998","unstructured":"Foley RN, Parfrey PS. 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