ArticleScientific reports2018
Hypoxia induces pulmonary fibroblast proliferation through NFAT signaling.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 89 citations in OpenAlex.
- The critical role of NFAT transcription factors in pulmonary arterial remodeling and pulmonary hypertension: from PASMC proliferation to therapeutic targeting.Molecular biology reports · 2026Review
- Fibroblasts as regulators of lung immunity, repair and fibrosis.Nature reviews. Immunology · 2026Review
- A retrospective analysis of paraquat and diquat poisoning: a single-center experience.Frontiers in medicine · 2026Article
- Simultaneous inhibition of ID1 and ID3 mitigates fibroblast activation via cell cycle and MEK/ERK pathways in pulmonary fibrosis.Theranostics · 2026Article
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- From Mechanoelectric Conversion to Tissue Regeneration: Translational Progress in Piezoelectric Materials.Advanced materials (Deerfield Beach, Fla.) · 2025Review
- Connexin 43 Affects Pulmonary Artery Reactivity via Changes in Nitric Oxide Production and Influences Proliferative and Migratory Responses in Mouse Pulmonary Artery Fibroblasts.International journal of molecular sciences · 2025Article
- Article
- Curcumin mediates oxidative stress to play an anti-fibrotic role, focusing on liver, renal, myocardial and pulmonary fibrosis.Frontiers in pharmacology · 2025Review
- CaBiomolecules · 2024Review
- Effects of Anti-Fibrotic Drugs on Transcriptome of Peripheral Blood Mononuclear Cells in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2024Article
- Use of Raman spectroscopy to study rat lung tissues for distinguishing asphyxia from sudden cardiac death.RSC advances · 2024Article
- Genetic deficiency of the transcription factor NFAT1 confers protection against fibrogenic responses independent of immune influx.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- The impact of hypoxia-inducible factors in the pathogenesis of kidney diseases: a link through cell metabolism.Kidney research and clinical practice · 2023Article
- NFATc3 Promotes Pulmonary Inflammation and Fibrosis by Regulating Production of CCL2 and CXCL2 in Macrophages.Aging and disease · 2023Article
- Review
- Endotyping COPD: hypoxia-inducible factor-2 as a molecular "switch" between the vascular and airway phenotypes?European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Hypoxia represses FOXF1 in lung endothelial cells through HIF-1α.Frontiers in physiology · 2023Article
- Effects of hypoxia on bronchial and alveolar epithelial cells linked to pathogenesis in chronic lung disorders.Frontiers in physiology · 2023Article
- Effect of Hypoxia in the Transcriptomic Profile of Lung Fibroblasts from Idiopathic Pulmonary Fibrosis.Cells · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and typically fatal lung disease with a very low survival rate. Excess accumulation of fibroblasts, myofibroblasts and extracellular matrix creates hypoxic conditions within the lungs, causing asphyxiation. Hypoxia is, therefore, one of the prominent features of IPF. However, there have been few studies concerning the effects of hypoxia on pulmonary fibroblasts. In this study, we investigated the molecular mechanisms of hypoxia-induced lung fibroblast proliferation. Hypoxia increased the proliferation of normal human pulmonary fibroblasts and IPF fibroblasts after exposure for 3-6 days. Cell cycle analysis demonstrated that hypoxia promoted the G1/S phase transition. Hypoxia downregulated cyclin D1 and A2 levels, while it upregulated cyclin E1 protein levels. However, hypoxia had no effect on the protein expression levels of cyclin-dependent kinase 2, 4, and 6. Chemical inhibition of hypoxia-inducible factor (HIF)-2 reduced hypoxia-induced fibroblast proliferation. Moreover, silencing of Nuclear Factor Activated T cell (NFAT) c2 attenuated the hypoxia-mediated fibroblasts proliferation. Hypoxia also induced the nuclear translocation of NFATc2, as determined by immunofluorescence staining. NFAT reporter assays showed that hypoxia-induced NFAT signaling activation is dependent on HIF-2, but not HIF-1. Furthermore, the inhibition or silencing of HIF-2, but not HIF-1, reduced the hypoxia-mediated NFATc2 nuclear translocation. Our studies suggest that hypoxia induces the proliferation of human pulmonary fibroblasts through NFAT signaling and HIF-2.
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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.