ArticleThe American journal of pathology2005
Modulation of prosurvival signaling in fibroblasts by a protein kinase inhibitor protects against fibrotic tissue injury.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.
- The bleomycin animal model: a useful tool to investigate treatment options for idiopathic pulmonary fibrosis?The international journal of biochemistry & cell biology · 2008Pooled it
- Targeting myeloid cell-mediated fibrosis through FAK.Nature biomedical engineering · 2026Article
- Loading of therapeutic cell penetrating peptides into extracellular vesicles for pulmonary fibrosis.Journal of controlled release : official journal of the Controlled Release Society · 2026Article
- Discoid Domain Receptors Signaling in Macrophages-Mediated Diseases.International journal of general medicine · 2025Review
- Integrated bioinformatics analysis identifies established and novel TGFβ1-regulated genes modulated by anti-fibrotic drugs.Scientific reports · 2022Article
- Modeling Kaempferol as a Potential Pharmacological Agent for COVID-19/PF Co-Occurrence Based on Bioinformatics and System Pharmacological Tools.Frontiers in pharmacology · 2022Article
- The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022Article
- Chrysin Ameliorates Cyclosporine-A-Induced Renal Fibrosis by Inhibiting TGF-βInternational journal of molecular sciences · 2021Article
- Mesenchymal stromal cell aging impairs the self-organizing capacity of lung alveolar epithelial stem cells.eLife · 2021Article
- Review
- PDGF-BB induces conversion, proliferation, migration, and collagen synthesis of oral mucosal fibroblasts through PDGFR-β/PI3K/ AKT signaling pathway.Cancer biomarkers : section A of Disease markers · 2021Article
- The Crosstalk between FAK and Wnt Signaling Pathways in Cancer and Its Therapeutic Implication.International journal of molecular sciences · 2020Review
- Liver epithelial focal adhesion kinase modulates fibrogenesis and hedgehog signaling.JCI insight · 2020Article
- Protein tyrosine phosphatase-α amplifies transforming growth factor-β-dependent profibrotic signaling in lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- PI3K-Akt-mTOR/PFKFB3 pathway mediated lung fibroblast aerobic glycolysis and collagen synthesis in lipopolysaccharide-induced pulmonary fibrosis.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Constitutive AKT Activity Predisposes Lung Fibrosis by Regulating Macrophage, Myofibroblast and Fibrocyte Recruitment and Changes in Autophagy.Advances in bioscience and biotechnology (Print) · 2019Article
- Role of fibroblast growth factor 23 and klotho cross talk in idiopathic pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Cell Death in the Lung: The Apoptosis-Necroptosis Axis.Annual review of physiology · 2019Review
- Mechanisms for the Resolution of Organ Fibrosis.Physiology (Bethesda, Md.) · 2019Review
- Discoidin Domain Receptor 2 Signaling Regulates Fibroblast Apoptosis through PDK1/Akt.American journal of respiratory cell and molecular biology · 2018Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Progressive fibrotic diseases involving diverse organ systems are associated with the persistence of fibroblasts/myofibroblasts in injured tissues. Activation of focal adhesion kinase (FAK) and protein kinase B (PKB/Akt) by transforming growth factor-beta1 mediate stable induction of myofibroblast differentiation and survival. In this report, we demonstrate that transforming growth factor-beta1-induced activation of both PKB/Akt and FAK are dose dependently inhibited by the protein kinase inhibitor, AG1879, in cultured human lung fibroblasts. In a murine model of intratracheal bleomycin-induced lung fibrosis, regions of active fibrogenesis demonstrate elevated expression of PKB/Akt and FAK phosphorylation in vivo, effects that are attenuated in mice receiving daily intraperitoneal injections of AG1879 (bleomycin-AG1879) versus a chemically inactive analog (bleomycin-control). PKB/Akt and FAK phosphorylation are elevated in fibroblasts isolated from lungs of bleomycin-injured mice, effects that are inhibited in bleomycin-AG1879 mice. Accumulation of alpha-smooth muscle actin-expressing myofibroblasts is markedly reduced in lungs of bleomycin-AG1879 mice. The numbers of recruited inflammatory cells were not significantly different between these groups. Bleomycin-AG1879 mice are protected from lung fibrosis as evidenced by histopathology, trichrome staining, and biochemical analysis for collagen. Thus, targeting of prosurvival signaling pathways in fibroblasts/myofibroblasts may provide a novel and effective strategy for anti-fibrotic therapy of treatment-unresponsive fibrotic disorders.
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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.