ArticleNature communications2023
Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 98 citations in OpenAlex.
- The Hallmarks of Aging: From Molecular Mechanisms to Clinical Translation.International journal of molecular sciences · 2026Review
- An Integrated DNA Nanoprobe for Intranuclear Imaging and In Situ Profiling of OGG1 Activity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Disease landscape-guided design of neutrophil-specific reporters for early and accurate pneumonia detection in vivo and in urine.Science advances · 2026Article
- Atg5 deficiency alters myofibroblast accumulation and alveolar regeneration in lung fibrosis.Stem cell reports · 2026Article
- Transcriptomics reveal dysregulated genes during folic acid-induced acute injury and fibrosis in kidney and their attenuation by antioxidantAmerican journal of physiology. Cell physiology · 2026Article
- Reparative "exosome-ark" for mitochondrial transplantation to reprogram macrophages and disrupt pathogenic crosstalk in pulmonary fibrosis.Materials today. Bio · 2026Article
- Article
- Exploring the role of RCEO in macrophage-mediated modulation of pulmonary fibrosis.Chinese medicine · 2026Article
- Facilitated DNA damage repair as an emerging therapeutic strategy for inflammatory and fibrotic diseases.RSC chemical biology · 2026Review
- Ogg1 regulates TGF‑β-Smad3 signalling and fibrosis progression in chronic kidney disease.Communications biology · 2026Article
- Epigenome-wide Mendelian randomization with multi-omics validation identifies epigenetic drivers of idiopathic pulmonary fibrosis.Communications biology · 2026Article
- Pathophysiological and therapeutic implications of C-type natriuretic peptide/cyclic GMP signaling in pulmonary fibrosis.JCI insight · 2026Article
- Control of airway basal stem cell-mediated lung repair by TGF-β signaling.Science advances · 2026Article
- Sbno2-mediated tissue-resident alveolar macrophages: a novel therapeutic axis for sepsis-induced acute lung injury.Cell death discovery · 2026Review
- An hiPSC-derived multi-lineage lung model exhibiting proximal-distal epithelial features for modeling pulmonary fibrosis.Frontiers in cell and developmental biology · 2026Article
- Integrated Approaches in Drug Repositioning Highlight Ouabain and Helenalin as Potential Drug Candidates for Pulmonary Fibrosis.Computational and structural biotechnology journal · 2026Article
- Hypoxia: a critical pathophysiological driver in respiratory inflammatory diseases.Military Medical Research · 2026Review
- Mitophagy in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Multi-omics analysis revealed coordinated responses of rumen microbiota and epithelium of goats to dietary supplementation of glucosamine selenium.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 3 countries.
Funding
Abstract
Interstitial lung diseases such as idiopathic pulmonary fibrosis (IPF) are caused by persistent micro-injuries to alveolar epithelial tissues accompanied by aberrant repair processes. IPF is currently treated with pirfenidone and nintedanib, compounds which slow the rate of disease progression but fail to target underlying pathophysiological mechanisms. The DNA repair protein 8-oxoguanine DNA glycosylase-1 (OGG1) has significant roles in the modulation of inflammation and metabolic syndromes. Currently, no pharmaceutical solutions targeting OGG1 have been utilized in the treatment of IPF. In this study we show Ogg1-targeting siRNA mitigates bleomycin-induced pulmonary fibrosis in male mice, highlighting OGG1 as a tractable target in lung fibrosis. The small molecule OGG1 inhibitor, TH5487, decreases myofibroblast transition and associated pro-fibrotic gene expressions in fibroblast cells. In addition, TH5487 decreases levels of pro-inflammatory mediators, inflammatory cell infiltration, and lung remodeling in a murine model of bleomycin-induced pulmonary fibrosis conducted in male C57BL6/J mice. OGG1 and SMAD7 interact to induce fibroblast proliferation and differentiation and display roles in fibrotic murine and IPF patient lung tissue. Taken together, these data suggest that TH5487 is a potentially clinically relevant treatment for IPF but further study in human trials is required.
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