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Biochem Cell Biol. 2015 Apr;93(2):109-18. doi: 10.1139/bcb-2014-0095. Epub 2014 Sep 18.

The role of miR-29 in pulmonary fibrosis.

Author information

1
The Columbia Center for Human Development, Division of Pulmonary, Allergy & Critical Care Medicine, Department of Medicine, Columbia University, College of Physicians & Surgeons, 630 West 168th Street, BB 8-810, New York, NY 10032, USA.

Abstract

Pulmonary fibrosis is a pathological condition in which lungs become scarred due to the excess extracellular matrix (ECM) deposition and structural alterations in the interstitium of lung parenchyma. Many patients with interstitial lung diseases (ILDs) caused by long-term exposure to toxic substances, chronic infections, or autoimmune responses develop fibrosis. Etiologies for many ILDs are unknown, such as idiopathic pulmonary fibrosis (IPF), a devastating, relentless form of pulmonary fibrosis with a median survival of 2-3 years. Despite several decades of research, factors that initiate and sustain the fibrotic response in lungs remain unclear and there is no effective treatment to block progression of fibrosis. Here we summarize recent findings on the antifibrotic activity of miR-29, a small noncoding regulatory RNA, in the pathogenesis of fibrosis by regulating ECM production and deposition, and epithelial-mesenchymal transition (EMT). We also describe interactions of miR-29 with multiple profibrotic and inflammatory pathways. Finally, we review the antifibrotic activity of miR-29 in animal models of fibrosis and highlight miR-29 as a promising therapeutic reagent or target for the treatment of pulmonary fibrosis.

KEYWORDS:

ECM-related genes; PDGF; TGFB; fibrose pulmonaire; gènes reliés à la MEC; interleukines; interleukins; miR-29; pulmonary fibrosis

PMID:
25454218
DOI:
10.1139/bcb-2014-0095
[Indexed for MEDLINE]

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