AI Article Synopsis
- 8-oxoguanine (8-oxoG) is a DNA lesion caused by reactive oxygen species that leads to genetic instability, and it's recognized by the repair protein OGG1.
- OGG1 plays a dual role in base excision repair and regulates gene expression, particularly during the activation of fibroblasts in lung fibrosis.
- Increasing OGG1 levels during fibroblast activation enhances pro-fibrotic gene expression in response to bleomycin, suggesting that targeting OGG1 could be a viable therapeutic strategy for treating Idiopathic Pulmonary Fibrosis (IPF).
Article Abstract
One of abundant DNA lesions induced by reactive oxygen species is 8-oxoguanine (8-oxoG), which compromises genetic instability. 8-oxoG is recognized by the DNA repair protein 8-oxoguanine DNA glycosylase-1 (OGG1) that not only participates in base excision repair but also involves in transcriptional regulation.OGG1 has an important role inIdiopathic Pulmonary Fibrosis (IPF) processing and targeting fibroblasts is a major strategy for the treatment of pulmonary fibrosis, but whether OGG1 activate fibroblast is not clear. In this study, we show that OGG1 expression level is increased at the fibroblast activation stage in mouse lungs induced by bleomycin (BLM) treatment. OGG1 promoted the expression level of fibroblast activation markers (CTGF, fibronectin, and collagen 1) in a pro-fibrotic gene transcriptional regulation pathway via interacting with Snail1, which dependent on 8-oxoG recognition. Global inhibition of OGG1 at the middle stage of lung fibrosis also relieved BLM-induced lung fibrosis in mice. Our results suggest that OGG1 is a target for inhibiting fibroblast activation and a potential therapeutic target for IPF.
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| http://dx.doi.org/10.1016/j.intimp.2023.111148 | DOI Listing |
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