Mechanisms of the alternative activation of macrophages and non-coding RNAs in the development of radiation-induced lung fibrosis.
Mechanisms of the alternative activation of macrophages and non-coding RNAs in the development of radiation-induced lung fibrosis.
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DOI：
10.4331/wjbc.v7.i4.231
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发表时间：
2016-11-26
期刊：
影响因子：
--
通讯作者：
Zhou Q
中科院分区：
文献类型：
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作者：
Duru N;Wolfson B;Zhou Q
放射性肺纤维化（RILF）是胸部放射治疗的常见副作用，并导致癌症治疗后的高死亡率。放射损伤诱导炎性M1巨噬细胞极化，导致放射性肺炎，RILF进展的第一阶段。纤维化的发生是由于M1巨噬细胞向抗炎促纤维化M2表型的转变，以及由此产生的巨噬细胞调节的炎症信号的不平衡。已显示非编码RNA信号传导在与纤维化的发展和进展相关的M2介导的信号传导途径的调节中发挥重要作用。虽然许多研究表明M2巨噬细胞和纤维化之间的联系，但只有少数研究探讨了它们的独特作用以及RILF中非编码RNA对其信号传导的调节。在这篇综述中，我们总结了目前的知识体系描述RILF中的M2巨噬细胞的作用，强调非编码RNA的表达和功能。
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.