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Phosphate: An old bone molecule but new cardiovascular risk factor

机译:磷酸盐:旧的骨分子,但新的心血管危险因素

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摘要

Phosphate handling in the body is complex and involves hormones produced by the bone, the parathyroid gland and the kidneys. Phosphate is mostly found in hydroxyapatite. however recent evidence suggests that phosphate is also a signalling molecule associated with bone formation. Phosphate balance requires careful regulation of gut and kidney phosphate transporters, SLC34 transporter family, but phosphate signalling in osteoblasts and vascular smooth muscle cells is likely mediated by the SLC20 transporter family (PiT1 and PiT2). If not properly regulated, phosphate imblanace could lead to mineral disorders as well as vascular calcification. In chronic kidney disease-mineral bone disorder, hyperphosphataemia has been consistently associated with extra-osseous 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. Finally, conventional as well as new and experimental therapeutics in the treatment of hyperphosphataemia are explored.
机译:体内的磷酸盐处理非常复杂,涉及骨骼,甲状旁腺和肾脏产生的激素。磷酸盐主要存在于羟基磷灰石中。然而,最近的证据表明磷酸盐也是与骨形成有关的信号分子。磷酸盐平衡需要仔细调节肠道和肾脏的磷酸盐转运蛋白,SLC34转运蛋白家族,但成骨细胞和血管平滑肌细胞中的磷酸信号可能是由SLC20转运蛋白家族(PiT1和PiT2)介导的。如果调节不当,磷酸盐im没可能会导致矿物质紊乱以及血管钙化。在慢性肾脏疾病-矿物骨疾病中,高磷血症一直与骨外钙化和心血管疾病有关。这篇综述着重于磷酸盐平衡和细胞信号传导(即成骨细胞和血管平滑肌细胞)所涉及的生理机制以及高磷血症的病理后果。最后,探索了治疗高磷血症的常规以及新型和实验性疗法。

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