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. 2019 Apr 16;17:35. doi: 10.1186/s12964-019-0347-1

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — The mechanism regulation of FOXM1 in pulmonary fibrosis. In response to various stimulus, such as inflammatory mediators, radiation and mitogen, FOXM1 induces the epithelial-to-mesenchymal transition in alveolar type II epithelial cells, and activates fibroblasts. Elevated FOXM1 transcription in activated fibroblasts promote the fibroblast proliferation, differentiation and DNA repair, consequently accelerating the process of pulmonary fibrosis. EC: endothelial cell; SMC: smooth muscle cell; CXCL12: chemokine ligand 12; CXCR4: chemokine receptor type 4; ET-1: endothelin-1; IGF-1: insulin-like growth factor-1; MIF: macrophage migration inhibitory factor; NBS1: Nijmegen breakage syndrome 1; PDGF-B: platelet-derived growth factor -B; PGE2: prostaglandin E2; BRCA2: breast cancer-associated gene 2