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. 2017 May 8;7:1554. doi: 10.1038/s41598-017-01765-6

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

A molecular system model for IPF. It involves four crucial biological pathways (Hedgehog signaling, Wnt signaling, TGFβ signaling and Cytokine-chemokine signaling) having cross-talk with each other. The model describes the mechanism and several regulatory components involved in IPF disease mechanism causing increased cell proliferation, adhesion, reduced differentiation, altered apoptosis and epithelial to mesenchymal transition. DEGs Frizzled 5 receptor, LTBP1, HHIP, BOC, CXCL12, CXCL14, ARRB1, NBL1 and SOCS3 appeared critical in IPF.