Suppr超能文献

[骨保护素及κB转录因子激活剂受体可溶性配体在主动脉瓣钙化中的表达]

[Expression of osteoprotegerin and soluble ligand of receptor of kappa-B transcription factor activator in the calcification of aortic valve].

作者信息

Voronkina I V, Irtyuga O B, Smagina L V, Adamova P E, Zhiduleva E V, Malashicheva A B, Sibagatullina Y S, Kruk L P, Gordeev M L, Moiseeva O M

机构信息

Institute of Cytology RAS, St. Petersburg, Russia.

Almazov National Medical Research Centre, St. Petersburg, Russia.

出版信息

Biomed Khim. 2019 Jan;65(1):57-62. doi: 10.18097/PBMC20196501057.

Abstract

The mechanism of valve calcification that is the main cause of aortic stenosis formation and progression is not yet clear. In recent years, the role of the OPG/RANKL/RANK system is considered as one of possible variants of pathogenesis of valve calcification. In presented work the differences in OPG and sRANKL levels involved in the calcification processes in tissues of patients with severe aortic stenosis have been examined. The study was performed using three groups of patients: group 1 - patients with aortic stenosis, group 2 - patients with aortic aneurysm, and group 3 - patients with aortic stenosis and aortic dilatation. In patients with aortic stenosis, the level of RANKL was significantly higher, and the level of RANKL was higher in valve than in tissue. The negative correlation between aortic dilatation and RANKL level indicated the lack of RANKL influence on pathogenesis of aortic dilatation. The obtained data confirm the increased expression of RANKL in patients with aortic valve calcification. The results of this study confirm importance of the OPG/RANKL/RANK system in calcification in patients with aortic stenosis. Athough patients of all groups had comparable values of OPG (including patients with aortic dilatation), the RANKL level increased only in patients with aortic stenosis. This suggest involvement of some additional mechanisms influencing the increase of RANKL expression.

摘要

瓣膜钙化是主动脉瓣狭窄形成和进展的主要原因,其机制尚不清楚。近年来,骨保护素/核因子κB受体活化因子配体/核因子κB受体活化因子(OPG/RANKL/RANK)系统的作用被认为是瓣膜钙化发病机制的可能变体之一。在本研究中,我们检测了重度主动脉瓣狭窄患者组织中参与钙化过程的OPG和可溶性RANKL(sRANKL)水平的差异。研究使用了三组患者:第1组——主动脉瓣狭窄患者;第2组——主动脉瘤患者;第3组——主动脉瓣狭窄合并主动脉扩张患者。在主动脉瓣狭窄患者中,RANKL水平显著升高,且瓣膜中的RANKL水平高于组织中的水平。主动脉扩张与RANKL水平呈负相关,表明RANKL对主动脉扩张的发病机制没有影响。所得数据证实了主动脉瓣钙化患者中RANKL表达增加。本研究结果证实了OPG/RANKL/RANK系统在主动脉瓣狭窄患者钙化中的重要性。尽管所有组患者的OPG值相当(包括主动脉扩张患者),但RANKL水平仅在主动脉瓣狭窄患者中升高。这表明存在一些影响RANKL表达增加的额外机制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验