Expression of osteoprotegerin and soluble ligand of receptor of kappa-B transcription factor activator in the calcification of aortic valve
Author(s) -
И. В. Воронкина,
O. B. Irtyuga,
Л. В. Смагина,
P. E. Adamova,
E. V. Zhiduleva,
Anna Malashicheva,
Yu. S. Sibagatullina,
Л. П. Крук,
Gordeev Mi,
О. М. Моисеева
Publication year - 2019
Publication title -
biomeditsinskaya khimiya
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.192
H-Index - 15
eISSN - 2310-6972
pISSN - 2310-6905
DOI - 10.18097/pbmc20196501057
Subject(s) - rankl , osteoprotegerin , stenosis , calcification , medicine , aortic valve , aortic valve stenosis , cardiology , pathogenesis , aorta , receptor , activator (genetics)
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.
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