解决难题：钙磷蛋白颗粒介导体矿物质转运。

Solving the insoluble: calciprotein particles mediate bulk mineral transport.

机构信息

Helmholtz-Institute for Biomedical Engineering, RWTH Aachen University Hospital, Aachen, Germany.

Department of Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria; Department of Nephrology, Lindenhofspital, Bern, Switzerland.

出版信息

Kidney Int. 2023 Apr;103(4):663-665. doi: 10.1016/j.kint.2023.01.011.

DOI:10.1016/j.kint.2023.01.011

PMID:36948767

Abstract

Protein mineral complexes, or calciprotein particles, are formed by calcium, phosphate, and the plasma protein fetuin-A. Crystalline calciprotein particles cause soft tissue calcification, oxidative stress, and inflammation, all well-known complications in chronic kidney disease. The T50 calcification propensity test measures how long it takes for amorphous calciprotein particles to crystallize. A study in this volume demonstrates remarkably low calcification propensity in cord blood, despite high mineral concentration. This hints to previously unidentified calcification inhibitors.

摘要

蛋白质矿物质复合物，或钙磷蛋白颗粒，由钙、磷酸盐和血浆蛋白胎球蛋白 A 组成。结晶钙磷蛋白颗粒可导致软组织钙化、氧化应激和炎症，这些都是慢性肾脏病的众所周知的并发症。T50 钙化倾向试验测量无定形钙磷蛋白颗粒结晶所需的时间。本期中的一项研究表明，尽管矿物质浓度高，但脐血的钙化倾向却非常低。这提示存在以前未识别的钙化抑制剂。