Osteoprotegerin/RANK/RANKL axis and atrial remodeling in mitral valvular patients with atrial fibrillation

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• 作者：Hailong Cao^a ; ¹ ; Qingguo Li^a ; ¹ ; Mingna Li^b ; Rø ; e OD^c ; ^d ; Zhong Wu^a ; Qing Zhou^a ; Bin Cao^a ; Baojun Chen^a ; Yijiang Chen^c ; Dongjin Wang^a ; ^{gldjw@163.com}
• 关键词：Atrial fibrillation ; Osteoprotegerin ; Receptor activator of nuclear factor-¦ÊB ; Receptor activator of nuclear factor-¦ÊB ligand ; Atrial remodeling
• 刊名：International Journal of Cardiology
• 出版年：2013
• 出版时间：1 July, 2013
• 年：2013
• 卷：166
• 期：3
• 页码：702-708
• 全文大小：1149 K

文摘

Background

Atrial remodeling is considered as the structural basis for the development and sustaining of atrial fibrillation (AF). Osteoprotegerin (OPG)/receptor activator of nuclear factor-¦ÊB (RANK)/RANK ligand (RANKL) axis, a key regulatory system in bone metabolism, was recently identified in some cardiovascular disorders for its regulation to myocardial remodeling. We hypothesized that the OPG/RANK/RANKL axis is involved in development and perpetuation of AF by regulating atrial remodeling.

Methods

Biopsies of right atrial appendage and clinical data were collected from sex- and age-matched 24 persistent AF, 24 paroxysmal AF, 24 sinus rhythm (SR) patients undergoing isolated mitral valve surgery and 24 healthy heart donors (normal controls).

Results

A significantly increasing gradient of atrial expression of OPG, RANKL, RANK and RANKL/OPG ratio was identified in normal controls, SR and AF groups. RANKL/OPG ratio was also found significantly higher in paroxysmal AF than persistent AF. Furthermore, atrial expression and activity of the axis was statistically correlated with collagen III/I levels and ratio and the degree of interstitial fibrosis reflected by collagen volume fraction in right atrial appendages.

Conclusions

The present findings suggest a potential role for known mediators of bone homeostasis in the pathogenesis of AF and possibly represent new targets for therapeutic intervention in AF.