ArticleBiomolecules2025
GSR Deficiency Exacerbates Oxidative Stress and Promotes Pulmonary Fibrosis.
Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Article
- Research on Therapeutic Strategy of Inhalable Cell Membrane-Coated Nanodelivery Complexes Mediating Nrf2 Pathway for Ameliorating Pulmonary Fibrosis.ACS applied materials & interfaces · 2026Article
- Identification of candidate selenium-associated transcriptomic biomarkers in chronic obstructive pulmonary disease: an integrated bioinformatics and expression validation study.Frontiers in medicine · 2026Article
- A regulatory network underlying idiopathic pulmonary fibrosis.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disorder characterized by excessive scarring of lung tissue, predominantly affecting middle-aged and elderly populations. Oxidative stress plays a pivotal role in the pathogenesis of pulmonary fibrosis, disrupting redox homeostasis and driving fibrotic progression. Glutathione reductase (GSR), a key antioxidant enzyme, is essential for maintaining cellular glutathione (GSH) levels and mitigating oxidative damage. However, the specific involvement of GSR in IPF remains poorly understood. This study found that GSR levels were downregulated in IPF patients and mice treated with bleomycin (BLM). GSR knockdown enhanced epithelial-to-mesenchymal transition (EMT) in A549 cells and promoted the activation of MRC5 cells. Additionally, GSR depletion promoted cellular migration and senescence in both A549 and MRC5 cells. Mechanistically, silencing GSR in A549 and MRC5 cells led to a marked reduction in intracellular GSH levels, resulting in elevated reactive oxygen species (ROS) accumulation, thereby promoting the activation of the TGF-β/Smad2 signaling pathway. In conclusion, our findings demonstrate that GSR deficiency aggravates pulmonary fibrosis by impairing antioxidant defense mechanisms, promoting EMT, and activating fibroblasts through the TGF-β/Smad2 signaling. These findings suggest that GSR may be essential in reducing the fibrotic progression of IPF.
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