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Phosphate balance requires careful regulation of gut and kidney phosphate transporters, <jats:styled-content style=\"fixed-case\">SLC<\/jats:styled-content>34 transporter family, but phosphate signalling in osteoblasts and vascular smooth muscle cells is likely mediated by the <jats:styled-content style=\"fixed-case\">SLC<\/jats:styled-content>20 transporter family (<jats:styled-content style=\"fixed-case\">PiT1<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">PiT2<\/jats:styled-content>). If not properly regulated, phosphate imblanace could lead to mineral disorders as well as vascular calcification. In chronic kidney disease\u2010mineral bone disorder, hyperphosphataemia has been consistently associated with extra\u2010osseous calcification and cardiovascular disease. This review focuses on the physiological mechanisms involved in phosphate balance and cell signalling (i.e. osteoblasts and vascular smooth muscle cells) as well as pathological consequences of hyperphosphataemia. 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