Role of MicroRNAs in Fibrosis



Serena Vettori 1, 2, Steffen Gay 1, Oliver Distler*, 1
1 Center of Experimental Rheumatology, ZIHP, University Hospital Zurich, Gloriastrasse 25, CH-8091 Zurich, Switzerland
2 Department of Clinical Medicine, Cardiovascular and Immunologic Sciences, University of Naples “Federico II”, via Pansini 5, 80131 I-Naples, Italy


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© Vettori et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the University Hospital Zurich, Gloriastrasse 25, 8091 Zurich, Switzerland; Tel: +41-44-255-2977; Fax: +41-44-255-4170; E-mail: oliver.distler@usz.ch


Abstract

Fibrosis is the leading cause of organ dysfunction in diseases such as systemic sclerosis, liver cirrhosis, cardiac fibrosis, progressive kidney disease, and idiopathic pulmonary fibrosis. The hallmark of fibrosis is tissue remodeling with excess deposition of extracellular matrix components, predominantly collagens. Different cell types, cytokines, growth factors, and enzymes interact in complex pathogenic networks with myofibroblasts playing a pivotal role. MicroRNAs are small non-coding RNAs acting as negative regulators of gene expression at the post-transcriptional level. MicroRNAs have been associated with many basic cellular processes as well as with a wide spectrum of diseases, most notably cancer. This review provides a comprehensive overview of microRNAs regulating profibrotic pathways and extracellular matrix synthesis. The potential of miRNA for targeted therapeutic approaches in fibrotic disorders is also discussed.

Keywords: Fibrosis, fibroblasts, microRNA (miRNA)-mediated gene regulation regulation, transforming growth factor-beta (TGF-β), connective tissue growth factor (CTGF), extracellular matrix (ECM), epithelial-to-mesenchymal transition (EMT), signaling pathways, antagomirs..