ArticleCell death & disease2013
Histone modifications are responsible for decreased Fas expression and apoptosis resistance in fibrotic lung fibroblasts.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 147 citations in OpenAlex.
- Climate Change and the Impact On Interstitial Lung Diseases.Pulmonary therapy · 2026Review
- Conditional BCL-2 Expression in Fibroblasts Promotes Persistent Pulmonary Fibrosis which is Reversible by Therapeutic BCL-2 Inhibition.Nature communications · 2026Article
- The Fibrotic-Cancer Continuum in IPF: Shared Mechanisms, Clinical Implications and Therapeutic Challenges.Life (Basel, Switzerland) · 2026Review
- Therapeutic Potential of Cannabinoids in Attenuating Amiodarone-Induced Pulmonary Fibrosis: An in vivo Experimental Study in Wistar Rats.Drug design, development and therapy · 2026Article
- Reversal of Myofibroblast Apoptosis Resistance and Collagen Deposition by Phaseoloidin-Induced Autophagy Attenuates Pulmonary Fibrosis.Biomedicines · 2025Article
- Targeting Dermal Fibroblast Senescence: From Cellular Plasticity to Anti-Aging Therapies.Biomedicines · 2025Review
- Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases.BMB reports · 2025Review
- Air pollution and alveolar health.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- R5S4TRAIL ameliorates radiation-induced pulmonary fibrosis by alleviating inflammatory responses and promoting apoptosis of fibroblasts.Frontiers in immunology · 2025Article
- SAHA inhibits lung fibroblast activation by increasing p66Shc expression epigenetically.Aging medicine (Milton (N.S.W)) · 2024Article
- Profibrotic role of the SOX9-MMP10-ECM biosynthesis axis in the tracheal fibrosis after injury and repair.Genes & diseases · 2024Article
- Biomarkers in idiopathic pulmonary fibrosis: Current insight and future direction.Chinese medical journal pulmonary and critical care medicine · 2024Article
- Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024Review
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- The evolution ofEuropean respiratory review : an official journal of the European Respiratory Society · 2024Review
- The involvement of HDAC3 in the pathogenesis of lung injury and pulmonary fibrosis.Frontiers in immunology · 2024Review
- Histone deacetylases: potential therapeutic targets for idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Histone Deacetylase 1 Inhibition by Peptides Containing a DNA Damage-Induced, Nonenzymatic, Histone Covalent Modification.Biochemistry · 2023Article
- Review
25 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Although the recruitment of fibroblasts to areas of injury is critical for wound healing, their subsequent apoptosis is necessary in order to prevent excessive scarring. Fibroproliferative diseases, such as pulmonary fibrosis, are often characterized by fibroblast resistance to apoptosis, but the mechanism(s) for this resistance remains elusive. Here, we employed a murine model of pulmonary fibrosis and cells from patients with idiopathic pulmonary fibrosis (IPF) to explore epigenetic mechanisms that may be responsible for the decreased expression of Fas, a cell surface death receptor whose expression has been observed to be decreased in pulmonary fibrosis. Murine pulmonary fibrosis was elicited by intratracheal injection of bleomycin. Fibroblasts cultured from bleomycin-treated mice exhibited decreased Fas expression and resistance to Fas-mediated apoptosis compared with cells from saline-treated control mice. Although there were no differences in DNA methylation, the Fas promoter in fibroblasts from bleomycin-treated mice exhibited decreased histone acetylation and increased histone 3 lysine 9 trimethylation (H3K9Me3). This was associated with increased histone deacetylase (HDAC)-2 and HDAC4 expression. Treatment with HDAC inhibitors increased Fas expression and restored susceptibility to Fas-mediated apoptosis. Fibroblasts from patients with IPF likewise exhibited decreased histone acetylation and increased H3K9Me3 at the Fas promoter and increased their expression of Fas in the presence of an HDAC inhibitor. These findings demonstrate the critical role of histone modifications in the development of fibroblast resistance to apoptosis in both a murine model and in patients with pulmonary fibrosis and suggest novel approaches to therapy for progressive fibroproliferative disorders.
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