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Review

Non-coding RNAs as direct and indirect modulators of epigenetic mechanism regulation of cardiac fibrosis

, MD, , MD & , PhD
Pages 707-716 | Published online: 04 Feb 2015
 

Abstract

Introduction: Cardiac fibroblast activation is a pivotal cellular event in cardiac fibrosis. Numerous studies have indicated that epigenetic modifications control cardiac fibroblast activation. Greater knowledge of the role of epigenetic modifications could improve understanding of the cardiac fibrosis pathogenesis.

Areas covered: The aim of this review is to describe the present knowledge about the important role of non-coding RNA (ncRNA) transcripts in epigenetic gene regulation in cardiac fibrosis and looks ahead on new perspectives of epigenetic modification research. Furthermore, we will discuss examples of ncRNAs that interact with histone modification or DNA methylation to regulate gene expression.

Expert opinion: MicroRNAs (miRNAs) and long ncRNAs (lncRNAs) modulate several important aspects of function. Recently, some studies continue to find novel pathways, including the important role of ncRNA transcripts in epigenetic gene regulation. Targeting the miRNAs and lncRNAs can be a promising direction in cardiac fibrosis treatment. We discuss new perspectives of ncRNAs that interact with histone modification or DNA methylation to regulate gene expression, others that are targets of these epigenetic mechanisms. The emerging recognition of the diverse functions of ncRNAs in regulating gene expression by epigenetic mechanisms suggests that they may represent new targets for therapeutic intervention.

Declaration of interest

The authors were supported by Anhui Provincial Natural Science Foundation (1408085MH175, 1308085MH117) and Anhui Medical University Foundation (2015xkj014). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

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