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The MicroRNA miR-155 Is Essential in Fibrosis

Department of Microbiology & Immunology, Drexel University College of Medicine, Drexel University, 2900 Queen Lane, Philadelphia, PA 19129, USA
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Author to whom correspondence should be addressed.
Non-Coding RNA 2019, 5(1), 23; https://doi.org/10.3390/ncrna5010023
Received: 31 January 2019 / Revised: 4 March 2019 / Accepted: 7 March 2019 / Published: 12 March 2019
The function of microRNAs (miRNAs) during fibrosis and the downstream regulation of gene expression by these miRNAs have become of great biological interest. miR-155 is consistently upregulated in fibrotic disorders, and its ablation downregulates collagen synthesis. Studies demonstrate the integral role of miR-155 in fibrosis, as it mediates TGF-β1 signaling to drive collagen synthesis. In this review, we summarize recent findings on the association between miR-155 and fibrotic disorders. We discuss the cross-signaling between macrophages and fibroblasts that orchestrates the upregulation of collagen synthesis mediated by miR-155. As miR-155 is involved in the activation of the innate and adaptive immune systems, specific targeting of miR-155 in pathologic cells that make excessive collagen could be a viable option before the depletion of miR-155 becomes an attractive antifibrotic approach. View Full-Text
Keywords: miR-155; fibrosis; inflammasome; fibroblasts; TGF-β1 miR-155; fibrosis; inflammasome; fibroblasts; TGF-β1
MDPI and ACS Style

Eissa, M.G.; Artlett, C.M. The MicroRNA miR-155 Is Essential in Fibrosis. Non-Coding RNA 2019, 5, 23. https://doi.org/10.3390/ncrna5010023

AMA Style

Eissa MG, Artlett CM. The MicroRNA miR-155 Is Essential in Fibrosis. Non-Coding RNA. 2019; 5(1):23. https://doi.org/10.3390/ncrna5010023

Chicago/Turabian Style

Eissa, Mousa G.; Artlett, Carol M. 2019. "The MicroRNA miR-155 Is Essential in Fibrosis" Non-Coding RNA 5, no. 1: 23. https://doi.org/10.3390/ncrna5010023

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Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

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