title: Mechanisms of the alternative activation of macrophages and non-coding RNAs in the development of radiation-induced lung fibrosis.
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.
authors.affiliation: Nadire Duru, Benjamin Wolfson, Qun Zhou, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, United States.
authors.forename: Nadire
authors.initials: N
authors.lastname: Duru
authors.affiliation: Nadire Duru, Benjamin Wolfson, Qun Zhou, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, United States.
authors.forename: Benjamin
authors.initials: B
authors.lastname: Wolfson
authors.affiliation: Nadire Duru, Benjamin Wolfson, Qun Zhou, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, United States.
authors.forename: Qun
authors.initials: Q
authors.lastname: Zhou
keywords: Fibrosis; Long-noncoding RNAs; M1; M2; Macrophages; MicroRNA; Non-coding RNA; Radiation-induced lung fibrosis