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[高磷血症在血管钙化中的作用]

[Roles of hyperphosphatemia in vascular calcification].

作者信息

Shioi Atsushi, Nishizawa Yoshiki

机构信息

Osaka City University Graduate School of Medicine, Department of Cardiovascular Medicine.

出版信息

Clin Calcium. 2009 Feb;19(2):180-5.

Abstract

Derangemenst of mineral metabolism including hyperphosphatemia occur along with progression of chronic kidney disease (CKD) . Recent clinical studies suggest that hyperphosphatemia is a major risk factor for vascular calcification and cardiovascular mortality in dialysis patients. Two pathophysiological processes are involved in the development of vascular calcification : apoptosis and phenotypic transition to chondrocytes or osteoblasts (chondro-/osteogenic differentiation) . Inorganic phosphate has been demonstrated to induce apoptosis and calcification of vascular smooth muscle cells through inhibiting gas6/Axl/PI3K/Akt pathway (cell survival pathway) . Moreover, inorganic phosphate has been shown to promote in vitro calcification of vascular wall cells by stimulating osteoblastic differentiation through a type III sodium-dependent phosphate co-transporter (PiT-1) . These molecular mechanisms suggest that hyperphosphatemia may play a pivotal role in progression of vascular calcification in CKD.

摘要

随着慢性肾脏病(CKD)的进展会出现包括高磷血症在内的矿物质代谢紊乱。最近的临床研究表明,高磷血症是透析患者血管钙化和心血管死亡的主要危险因素。血管钙化的发生涉及两个病理生理过程:细胞凋亡以及向软骨细胞或成骨细胞的表型转变(软骨/成骨分化)。无机磷酸盐已被证明可通过抑制gas6/Axl/PI3K/Akt途径(细胞存活途径)诱导血管平滑肌细胞凋亡和钙化。此外,无机磷酸盐已显示可通过III型钠依赖性磷酸盐共转运蛋白(PiT-1)刺激成骨细胞分化来促进血管壁细胞的体外钙化。这些分子机制表明,高磷血症可能在CKD血管钙化的进展中起关键作用。

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