ArticleThe American journal of pathology2009
Notch1 signaling in FIZZ1 induction of myofibroblast differentiation.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 124 citations in OpenAlex.
- TKT inhibition attenuates cardiac fibrosis in myocardial infarction through deactivating AKT signaling pathway.Journal of translational medicine · 2026Article
- Airway Goblet Metaplasia Resulting from YAP/TAZ Deletion Drives Pulmonary Inflammatory Responses.American journal of respiratory cell and molecular biology · 2026Article
- CD206Circulation · 2025Article
- Epithelial Cell Dysfunction in Pulmonary Fibrosis: Mechanisms, Interactions, and Emerging Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Complex Interplay of TGF-β and Notch Signaling in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2024Review
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- The Role of Macrophages in Lung Fibrosis and the Signaling Pathway.Cell biochemistry and biophysics · 2024Review
- Single-Cell Transcriptomic Profiling Identifies Molecular Phenotypes of Newborn Human Lung Cells.Genes · 2024Article
- The mechanism of gut-lung axis in pulmonary fibrosis.Frontiers in cellular and infection microbiology · 2024Review
- Transformation of macrophages into myofibroblasts in fibrosis-related diseases: emerging biological concepts and potential mechanism.Frontiers in immunology · 2024Review
- Review
- Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023Review
- The histone methyltransferase DOT1L is a new epigenetic regulator of pulmonary fibrosis.Cell death & disease · 2022Article
- Article
- Notch3: A New Culprit in Fibrotic Lung Disease.American journal of respiratory cell and molecular biology · 2021Article
- The Role of Hypoxia-Induced Mitogenic Factor in Organ-Specific Inflammation in the Lung and Liver: Key Concepts and Gaps in Knowledge Regarding Molecular Mechanisms of Acute or Immune-Mediated Liver Injury.International journal of molecular sciences · 2021Review
- Potential functions of embryonic cardiac macrophages in angiogenesis, lymphangiogenesis and extracellular matrix remodeling.Histochemistry and cell biology · 2021Article
- Hypoxia-Induced Mitogenic Factor: A Multifunctional Protein Involved in Health and Disease.Frontiers in cell and developmental biology · 2021Review
- Disruption of myofibroblastic Notch signaling attenuates liver fibrosis by modulating fibrosis progression and regression.International journal of biological sciences · 2021Article
- YAP/TAZ affects the development of pulmonary fibrosis by regulating multiple signaling pathways.Molecular and cellular biochemistry · 2020Review
12 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 2 institutions in 1 country.
Funding
Abstract
Notch1 is an evolutionarily conserved receptor that regulates cell fate, including such events as differentiation, proliferation, and apoptosis. Myofibroblast differentiation is a key feature of lung fibrosis. Found in inflammatory zone 1 (FIZZ1) has direct fibrogenic properties because of its ability to induce myofibroblast differentiation. However, the downstream signaling pathway that mediates FIZZ1 induction of myofibroblast differentiation remains unknown. The objective of this study was to investigate the involvement of Notch signaling in FIZZ1 induction of lung myofibroblast differentiation and thus explore the potential role of Notch1 in pulmonary fibrosis. The results showed that FIZZ1 increased the expression levels of activated intracellular domain of Notch1 (NIC), its ligand Jagged1, and its target gene Hes1, which were associated with elevated alpha-smooth muscle actin expression levels. Fibroblast alpha-smooth muscle actin expression is induced by the overexpression of NIC but is suppressed by the inhibition of NIC. Moreover, lung fibroblasts that were isolated from mice lacking the GDP-4-keto-6-deoxymannose3,5-epimerase-4-reductase enzyme (FX knockout) exhibited significantly reduced responsiveness to FIZZ1, which was reversed by fucose supplementation. In the absence of exogenous fucose, these FX-deficient cells exhibited defective fucosylation, which is required for Notch signaling. These knockout mice also showed impaired lung fibrosis. These findings suggest that Notch1 signaling in response to FIZZ1 may play a significant role in myofibroblast differentiation during lung fibrosis.
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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.