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. 2023 Feb 6;14:643. doi: 10.1038/s41467-023-36314-5

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© The Author(s) 2023

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/.

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Fig. 8 — a Murine lung immunofluorescence analysis showed decreased levels of immunoreactivity for OGG1 (red)/SMAD7 (green) in TH5487 (TH)-treated mice compared to bleomycin (Bleo) controls (DAPI, blue; scale bar = 50 μm), results shown from 3 independent experiments, b with mouse lung homogenate samples analyzed by SDS-PAGE, followed by immunoblotting using rabbit antisera specific to OGG1 and SMAD7 (protein levels quantified inset n = 3 per treatment; statistical analyses were conducted using a one-way ANOVA (****P < 0.0001 for comparisons between all groups tested)). Data are presented as means ± SEM (b, c). c This result translated into human patient samples, with healthy control lung tissue displaying significantly decreased levels of OGG1 and SMAD7 immunoreactivity (brown staining; P = 0.0024 and P = 0.0002, respectively), as compared using an unpaired t test with Welch’s correction (two-sided), n = 4 patients per group. Scale bar = 6 mm and 100 μm for inset images. d Excessive OGG1 production facilitates pro-inflammatory gene expression, promoting inflammatory cell recruitment, leading to further exacerbation of the fibrotic lung environment. In addition, OGG1 promotes the phosphorylation of SMAD 2/3 by SMAD7 interaction, promoting TGF-β-driven FMT and EMT and excessive ECM deposition. Therefore, decreased OGG1 expression and binding to DNA by TH5487 inhibits downstream pro-inflammatory gene expression and pulmonary fibrosis. In this study, OGG1 and SMAD7 levels were both reduced after the administration of TH5487, as shown by SDS-page/immunoblotting. Source data are provided as a Source data file. Elements of this figure were created with BioRender.com.