骨型组织非特异性碱性磷酸酶和PHOSPO1在血管钙化中的作用。
Role of bone-type tissue-nonspecific alkaline phosphatase and PHOSPO1 in vascular calcification.
作者信息
Bobryshev Yuri V, Orekhov Alexander N, Sobenin Igor, Chistiakov Dimitry A
机构信息
Department of Medical Nanobiotechnology, Pirogov Russian State Medical University, 1 Ostrovityanova Str., 117997 Moscow, Russia.
出版信息
Curr Pharm Des. 2014;20(37):5821-8. doi: 10.2174/1381612820666140212193011.
Matrix vesicle (MV)-mediated mineralization is important for bone ossification. However, under certain circumstances such as atherosclerosis, mineralization may occur in the arterial wall. Bone-type tissue-nonspecific alkaline phosphatase (TNAP) hydrolyzes inorganic pyrophosphate (PPi) and generates inorganic phosphate (Pi), which is essential for MV-mediated hydroxyapatite formation. MVs contain another phosphatase, PHOSPHO1, that serves as an additional supplier of Pi. Activation of bone-type tissue-nonspecific alkaline phosphatase (TNAP) in vascular smooth muscle cells precedes vascular calcification. By degrading PPi, TNAP plays a procalcific role changing the Pi/PPi ratio toward mineralization. A pathologic role of bone-type TNAP and PHOSPHO1 make them to be attractive targets for cardiovascular therapy.
基质小泡（MV）介导的矿化作用对骨化很重要。然而，在某些情况下，如动脉粥样硬化，矿化可能发生在动脉壁。骨型组织非特异性碱性磷酸酶（TNAP）水解无机焦磷酸（PPi）并生成无机磷酸盐（Pi），这对MV介导的羟基磷灰石形成至关重要。MV含有另一种磷酸酶PHOSPHO1，它作为Pi的额外供应者。血管平滑肌细胞中骨型组织非特异性碱性磷酸酶（TNAP）的激活先于血管钙化。通过降解PPi，TNAP发挥促钙化作用，使Pi/PPi比值向矿化方向变化。骨型TNAP和PHOSPHO1的病理作用使其成为心血管治疗的有吸引力的靶点。
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