ReviewAntioxidants (Basel, Switzerland)2022
The Role of DNA Damage and Repair in Idiopathic Pulmonary Fibrosis.
Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 31 citations in OpenAlex.
- Harmine Derivative H-2-104 Alleviates Echinococcus granulosus-Induced Pulmonary Fibrosis in Mice by Inhibiting Fibroblast Activation and Inducing DNA Damage.Journal of immunology research · 2026Article
- DNA damage response and cell fate decisions across the lifespan: from fetal development to age-related respiratory diseases.Cell & bioscience · 2025Review
- Integrative analysis of gene expression and chromatin dynamics multi-omics data in mouse models of bleomycin-induced lung fibrosis.Epigenetics & chromatin · 2025Article
- Diagnostic and predictive values of m5C‑associated genes in idiopathic pulmonary fibrosis.Molecular medicine reports · 2025Article
- HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats.BMC pulmonary medicine · 2025Article
- Cardiac protection of wogonin in mice with pulmonary fibrosis by regulating Sirt1/ γ-H2AX pathway.Frontiers in pharmacology · 2025Article
- NR2F2 alleviates pulmonary fibrosis by inhibition of epithelial cell senescence.Respiratory research · 2024Article
- Cellular Senescence: A Troy Horse in Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Identification and validation of targets of swertiamarin on idiopathic pulmonary fibrosis through bioinformatics and molecular docking-based approach.BMC complementary medicine and therapies · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The mortality rate of idiopathic pulmonary fibrosis (IPF) increases yearly due to ineffective treatment. Given that the lung is exposed to the external environment, it is likely that oxidative stress, especially the stimulation of DNA, would be of particular importance in pulmonary fibrosis. DNA damage is known to play an important role in idiopathic pulmonary fibrosis initiation, so DNA repair systems targeting damage are also crucial for the survival of lung cells. Although many contemporary reports have summarized the role of individual DNA damage and repair pathways in their hypotheses, they have not focused on idiopathic pulmonary fibrosis. This review, therefore, aims to provide a concise overview for researchers to understand the pathways of DNA damage and repair and their roles in IPF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.