Research Paper|Volume 11, Issue 2|pp 448—466

miRNA-mRNA crosstalk in myocardial ischemia induced by calcified aortic valve stenosis

Chenyang Duan^1,², Zhezhe Cao², Fuqin Tang², Zhao Jian², Chunshui Liang², Hong Liu², Yingbin Xiao², Liangming Liu¹, Ruiyan Ma²

¹State Key Laboratory of Trauma, Burns and Combined Injury, Second Department of Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing, 400042, P. R. China
²Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Chongqing 400037, P. R. China

Received: October 1, 2018Accepted: December 27, 2018Published: January 16, 2019

https://doi.org/10.18632/aging.101751

Copyright: © 2019 Duan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Aortic valve stenosis is the most common cause of morbidity and mortality in valvular heart disease in aged people. Both microRNA (miRNA) and mRNA are potential targets for the diagnosis and therapeutic intervention of myocardial ischemia induced by calcified aortic valve stenosis (CAVS), with unclear mechanisms. Here, 3 gene expression profiles of 47 male participants were applied to generate shared differentially expressed genes (DEGs) with significant major biological functions. Moreover, 20 hub genes were generated by a Weighted Genes Co-Expression Network Analysis (WGCNA) and were cross-linked to miRNA based on miRanda/miRwalk2 databases. Integrated miRNA/mRNA analysis identified several novel miRNAs and targeted genes as diagnostic/prognostic biomarkers or therapeutic targets in CAVS patients. In addition, the clinical data suggested that myocardial hypertrophy and myocardial ischemia in CAVS patients are likely associated with hub genes and the upstream regulatory miRNAs. Together, our data provide evidence that miRNAs and their targeted genes play an important role in the pathogenesis of myocardial hypertrophy and ischemia in patients with CAVS.