ArticleThe Journal of pathology2016
Idiopathic pulmonary fibrosis fibroblasts become resistant to Fas ligand-dependent apoptosis via the alteration of decoy receptor 3.
Article in The Journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 48 citations in OpenAlex.
- Circulating levels of TL1A and its decoy receptor DcR3 in systemic sclerosis.Clinical rheumatology · 2026Article
- Ac-SDKP modulates apoptosis via HSP27 and the FAS/FASL and mitochondrial axes.Animal models and experimental medicine · 2026Article
- Differential Protective Actions of Dulaglutide and Dexamethasone in Methotrexate Induced Pulmonary Fibrosis: Relationship with AMPK and Beclin-1 Levels.Biomedicines · 2026Article
- Fibroblasts as regulators of lung immunity, repair and fibrosis.Nature reviews. Immunology · 2026Review
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.Oxidative medicine and cellular longevity · 2026Review
- Reversal of Myofibroblast Apoptosis Resistance and Collagen Deposition by Phaseoloidin-Induced Autophagy Attenuates Pulmonary Fibrosis.Biomedicines · 2025Article
- The lung microbiome in interstitial lung disease.Breathe (Sheffield, England) · 2025Review
- Combination therapy blocking TNF superfamily members 14 and 15 reverses pulmonary fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Proteomic Biomarkers of Survival in Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2024Article
- The aged extracellular matrix and the profibrotic role of senescence-associated secretory phenotype.American journal of physiology. Cell physiology · 2023Review
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- Review
- Functional Repercussions of Hypoxia-Inducible Factor-2α in Idiopathic Pulmonary Fibrosis.Cells · 2022Review
- Biomechanical Force and Cellular Stiffness in Lung Fibrosis.The American journal of pathology · 2022Review
- Transcriptional analysis of lung fibroblasts identifies PIM1 signaling as a driver of aging-associated persistent fibrosis.JCI insight · 2022Article
- Epigenetic Modifications in Tumor-Associated Macrophages: A New Perspective for an Old Foe.Frontiers in immunology · 2022Review
- Mitochondrial Dysfunction and Alterations in Mitochondrial Permeability Transition Pore (mPTP) Contribute to Apoptosis Resistance in Idiopathic Pulmonary Fibrosis Fibroblasts.International journal of molecular sciences · 2021Article
- Cellular Senescence: Pathogenic Mechanisms in Lung Fibrosis.International journal of molecular sciences · 2021Review
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is an irreversible lethal lung disease with an unknown etiology. IPF patients' lung fibroblasts express inappropriately high Akt activity, protecting them in response to an apoptosis-inducing type I collagen matrix. FasL, a ligand for Fas, is known to be increased in the lung tissues of patients with IPF, implicated with the progression of IPF. Expression of Decoy Receptor3 (DcR3), which binds to FasL, thereby subsequently suppressing the FasL-Fas-dependent apoptotic pathway, is frequently altered in various human disease. However, the role of DcR3 in IPF fibroblasts in regulating their viability has not been examined. We found that enhanced DcR3 expression exists in the majority of IPF fibroblasts on collagen matrices, resulting in the protection of IPF fibroblasts from FasL-induced apoptosis. Abnormally high Akt activity suppresses GSK-3β function, thereby accumulating the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) in the nucleus, increasing DcR3 expression in IPF fibroblasts. This alteration protects IPF cells from FasL-induced apoptosis on collagen. However, the inhibition of Akt or NFATc1 decreases DcR3 mRNA and protein levels, which sensitizes IPF fibroblasts to FasL-mediated apoptosis. Furthermore, enhanced DcR3 and NFATc1 expression is mainly present in myofibroblasts in the fibroblastic foci of lung tissues derived from IPF patients. Our results showed that when IPF cells interact with collagen matrix, aberrantly activated Akt increases DcR3 expression via GSK-3β-NFATc1 and protects IPF cells from the FasL-dependent apoptotic pathway. These findings suggest that the inhibition of DcR3 function may be an effective approach for sensitizing IPF fibroblasts in response to FasL, limiting the progression of lung fibrosis. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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