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World J Biol Chem. Nov 26, 2016; 7(4): 231-239
Published online Nov 26, 2016. doi: 10.4331/wjbc.v7.i4.231
Mechanisms of the alternative activation of macrophages and non-coding RNAs in the development of radiation-induced lung fibrosis
Nadire Duru, Benjamin Wolfson, Qun Zhou
Nadire Duru, Benjamin Wolfson, Qun Zhou, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, United States
Author contributions: Duru N and Wolfson B contributed equally to this manuscript; Duru N wrote the manuscript; Wolfson B wrote and reviewed the manuscript; Zhou Q designed the aim of the review and reviewed the manuscript.
Conflict-of-interest statement: There are no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Qun Zhou, MD, PhD, Associate Professor, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 North Greene Street, Baltimore, MD 21201, United States. qzhou@som.umaryland.edu
Telephone: +1-410-7061615 Fax: +1-410-7068297
Received: July 28, 2016
Peer-review started: July 31, 2016
First decision: September 2, 2016
Revised: September 17, 2016
Accepted: October 25, 2016
Article in press: October 27, 2016
Published online: November 26, 2016
Processing time: 112 Days and 20 Hours
Abstract

Radiation-induced lung fibrosis (RILF) is a common side effect of thoracic irradiation therapy and leads to high mortality rates after cancer treatment. Radiation injury induces inflammatory M1 macrophage polarization leading to radiation pneumonitis, the first stage of RILF progression. Fibrosis occurs due to the transition of M1 macrophages to the anti-inflammatory pro-fibrotic M2 phenotype, and the resulting imbalance of macrophage regulated inflammatory signaling. Non-coding RNA signaling has been shown to play a large role in the regulation of the M2 mediated signaling pathways that are associated with the development and progression of fibrosis. While many studies show the link between M2 macrophages and fibrosis, there are only a few that explore their distinct role and the regulation of their signaling by non-coding RNA in RILF. In this review we summarize the current body of knowledge describing the roles of M2 macrophages in RILF, with an emphasis on the expression and functions of non-coding RNAs.

Keywords: Macrophages; M1; M2; Non-coding RNA; MicroRNA; Long-noncoding RNAs; Radiation-induced lung fibrosis; Fibrosis

Core tip: We discuss the mechanisms of initiation and progression of radiation-induced lung fibrosis. First we summarize the role of M2 macrophages in the initiation and development of pulmonary fibrosis with an emphasis on their function in radiation-induced lung fibrosis. We then examine the growing evidence describing non-coding RNAs in the development and progression of radiation-induced lung fibrosis.