Lookup NU author(s): Emily Glover,
Professor Neil Sheerin,
Professor Simi Ali
This is the authors' accepted manuscript of an article that has been published in its final definitive form by Lippincott Williams & Wilkins, 2018.
For re-use rights please refer to the publisher's terms and conditions.
Fibrosis is a universal finding in chronic allograft dysfunction and is characterized by an accumulation of extracellular matrix. The precise source of the myofibroblasts responsible for matrix deposition is not understood and pharmacological strategies for prevention or treatment of fibrosis remain limited. One source of myofibroblasts in fibrosis is EndMT, a process first described in heart development. Recently, lineage tracing of endothelial cells in mouse models allowed studies of EndMT in vivo and reported 27-35% of myofibroblasts involved in cardiac fibrosis and 16% of isolated fibroblasts in bleomycin-induced pulmonary fibrosis to be of endothelial origin.Over the last decade, microRNAs have increasingly been described as key regulators of biological processes through repression or degradation of targeted mRNA. The stability and abundance of microRNAs in body fluids makes them attractive as potential biomarkers and progress is being made in developing microRNA targeted therapeutics. In this review we will discuss evidence of microRNA regulation of EndMT from in vitro and in vivo studies and the potential relevance of this to heart, lung and kidney allograft dysfunction.
Author(s): Glover EK, Jordan N, Sheerin NS, Ali S
Publication type: Article
Publication status: Published
Online publication date: 01/04/2019
Acceptance date: 09/12/2018
Date deposited: 18/12/2018
ISSN (print): 0041-1337
ISSN (electronic): 1534-6080
Publisher: Lippincott Williams & Wilkins
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