ArticleThe American journal of pathology2018
p53 Expression in Lung Fibroblasts Is Linked to Mitigation of Fibrotic Lung Remodeling.
Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
29 citing papers in PubMed, 38 citations in OpenAlex.
- Inhaled LTI-03 for idiopathic pulmonary fibrosis: a randomized dose escalation study.Nature communications · 2026Trial
- Targeting alveolar type II cell dysfunction in idiopathic pulmonary fibrosis: Molecular mechanisms and emerging therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Formononetin ameliorates bleomycin-induced pulmonary fibrosis in mice via targeting USP5.Journal of thoracic disease · 2026Article
- Therapeutic Potential of Cannabinoids in Attenuating Amiodarone-Induced Pulmonary Fibrosis: An in vivo Experimental Study in Wistar Rats.Drug design, development and therapy · 2026Article
- p53-miR-34a feedback in lung fibroblasts regulates antifibrotic effects of CSP7, nintedanib, and pirfenidone.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- LTI-03 peptide demonstrates anti-fibrotic activity iniScience · 2025Article
- Impact of Curcumin on the IL-17A-Mediated p53-Fibrinolytic System: Mouse Proteomics and Integrated Human Fibrosis scRNAseq Insights.Inflammation · 2025Article
- Comparative study of adipose tissue derived mesenchymal stem cells with rapamycin on paraquat-induced acute lung injury and pulmonary fibrosis in a mouse model: histological and biochemical study.Stem cell research & therapy · 2025Article
- Ratio of miRNA-29 to miRNA-199 expression coordinates mesenchymal stem cell repair of bleomycin-induced pulmonary injury.Molecular therapy. Nucleic acids · 2025Article
- Inhalable Carbonyl Sulfide Donor-Hybridized Selective Phosphodiesterase 10A Inhibitor for Treating Idiopathic Pulmonary Fibrosis by Inhibiting Tumor Growth Factor-β Signaling and Activating the cAMP/Protein Kinase A/cAMP Response Element-Binding Protein (CREB)/p53 Axis.ACS pharmacology & translational science · 2025Article
- p53 and the E3 Ubiquitin Ligase MDM2 in Glaucomatous Lamina Cribrosa Cells.International journal of molecular sciences · 2024Article
- Targeting tumor suppressor p53 for organ fibrosis therapy.Cell death & disease · 2024Review
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- Wogonin protects against bleomycin-induced mouse pulmonary fibrosis via the inhibition of CDK9/p53-mediated cell senescence.Frontiers in pharmacology · 2024Article
- FOXO4-D-Retro-Inverso targets extracellular matrix production in fibroblasts and ameliorates bleomycin-induced pulmonary fibrosis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023Review
- Review
- Local Delivery of Azithromycin Nanoformulation Attenuated Acute Lung Injury in Mice.Molecules (Basel, Switzerland) · 2022Article
- Caveolin-1 scaffolding domain peptide abrogates autophagy dysregulation in pulmonary fibrosis.Scientific reports · 2022Article
- Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a debilitating, incurable, and life-threatening disease. A cardinal feature of the pathogenesis of IPF is excessive extracellular matrix deposition attributable to proliferation of activated fibrotic lung fibroblasts (fLfs). To assess the underlying mechanism, we analyzed the status of the tumor suppressor protein p53 in fLfs from the lungs of IPF patients or mice with bleomycin-induced established PF. We report that basal expression of p53 is markedly reduced in fLfs. Forced expression of caveolin-1 in fLfs increased basal p53 and reduced profibrogenic proteins, including collagen-1. Transduction of fLfs with adenovirus expressing p53 reduced expression of these proteins. Conversely, inhibition of baseline p53 in control lung fibroblasts from lung tissues increased profibrogenic protein expression. Lung transduction of adenovirus expressing p53 reduced bleomycin-induced PF in wild-type or caveolin-1-deficient mice. Furthermore, treatment of fLfs or fibrotic lung tissues with caveolin-1 scaffolding domain peptide (CSP) or its fragment, CSP7, restored p53 and reduced profibrogenic proteins. Treatment of wild-type mice with i.p. CSP or CSP7 resolved bleomycin-induced PF. These peptides failed to resolve PF in inducible conditional knockout mice lacking p53 in fLfs, indicating the induction of baseline fLf p53 as the basis of the antifibrotic effects.
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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.