ArticleInternational journal of molecular sciences2024
IRF1 Mediates Growth Arrest and the Induction of a Secretory Phenotype in Alveolar Epithelial Cells in Response to Inflammatory Cytokines IFNγ/TNFα.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
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Who cites it
11 citing papers in PubMed, 9 citations in OpenAlex.
- Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFκB-dependent gene regulatory signatures.GeroScience · 2026Article
- Article
- IFNγ Increases Intracellular Amino Acid Content in Human Alveolar Epithelial Cells: Role of the STAT/IRF1 Axis in the Stimulation of Transmembrane Transport.International journal of molecular sciences · 2026Article
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Nagilactone C from the Seeds ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Deletion of PTHrP nuclear localization sequence and carboxyl terminus leads to lung dysplasia.Scientific reports · 2025Article
- Th1 Cytokines Inhibit Acinar Morphogenesis and Milk Protein Expression in 3D Mammary Cultures.Biomedicines · 2025Article
- Development of an acute lung injury model for drug testing.Scientific reports · 2025Article
- miR-1226-5p is involved in radioresistance of colorectal cancer by activating M2 macrophages through suppressing IRF1.Journal of translational medicine · 2024Article
- Cytokines from SARS-CoV-2 Spike-Activated Macrophages Hinder Proliferation and Cause Cell Dysfunction in Endothelial Cells.Biomolecules · 2024Article
- Transcription factor network dynamics during the commitment to oncogene-induced senescence.Frontiers in epigenetics and epigenomics · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In COVID-19, cytokine release syndrome can cause severe lung tissue damage leading to acute respiratory distress syndrome (ARDS). Here, we address the effects of IFNγ, TNFα, IL-1β and IL-6 on the growth arrest of alveolar A549 cells, focusing on the role of the IFN regulatory factor 1 (IRF1) transcription factor. The efficacy of JAK1/2 inhibitor baricitinib has also been tested. A549 WT and IRF1 KO cells were exposed to cytokines for up to 72 h. Cell proliferation and death were evaluated with the resazurin assay, analysis of cell cycle and cycle-regulator proteins, LDH release and Annexin-V positivity; the induction of senescence and senescence-associated secretory phenotype (SASP) was evaluated through β-galactosidase staining and the quantitation of secreted inflammatory mediators. While IL-1 and IL-6 proved ineffective, IFNγ plus TNFα caused a proliferative arrest in A549 WT cells with alterations in cell morphology, along with the acquisition of a secretory phenotype. These effects were STAT and IRF1-dependent since they were prevented by baricitinib and much less evident in IRF1 KO than in WT cells. In alveolar cells, STATs/IRF1 axis is required for cytokine-induced proliferative arrest and the induction of a secretory phenotype. Hence, baricitininb is a promising therapeutic strategy for the attenuation of senescence-associated inflammation.
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Registered trials
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