ArticleCells2022
Niclosamide Ethanolamine Salt Alleviates Idiopathic Pulmonary Fibrosis by Modulating the PI3K-mTORC1 Pathway.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Niclosamide as a Promising Therapeutic Player in Human Cancer and Other Diseases.International journal of molecular sciences · 2022Pooled it
- Research on the role and mechanism of SLC7A5 in idiopathic pulmonary fibrosis.Molecular medicine reports · 2026Article
- Beryllium Sulfate-Induced Cellular Senescence via the IL-6/STAT3 Pathway to Promote Pulmonary Fibrosis.Journal of applied toxicology : JAT · 2026Article
- Therapeutic Effect of Niclosamide versus Triamcinolone on Rabbit Ear Model of Hypertrophic Scar.Aesthetic plastic surgery · 2026Article
- Targeting mTORC1/TGFB1 signaling with a novel Bergapten-Esculetin combination: a computational and experimental approach in idiopathic pulmonary fibrosis.Molecular diversity · 2026Article
- DCLK1 mediates airway epithelial barrier disruption through NF-κB activation in severe asthma.Molecular medicine (Cambridge, Mass.) · 2026Article
- Defective branched-chain amino acid catabolism promotes pulmonary fibrosis by inducing apoptosis resistance of myofibroblasts in mice.Cell communication and signaling : CCS · 2026Article
- Yifei Decoction Regulates the NGF/TRKA/PI3K/AKT Signaling Axis to Inhibit the Epithelial-Mesenchymal Transformation and Proliferation of Pulmonary Epithelial Cells in Bleomycin-Induced Pulmonary Fibrogenesis.Canadian respiratory journal · 2026Article
- Cinobufotalin Ameliorates the Development of Pulmonary Fibrosis by Suppressing the TGF-β/Smad Pathway via Regulating PI15.Journal of cellular and molecular medicine · 2025Article
- Stem cell therapy for intervertebral disc degeneration: Clinical progress with exosomes and gene vectors.World journal of stem cells · 2025Review
- Cromolyn sodium reduces LPS-induced pulmonary fibrosis by inhibiting the EMT process enhanced by MC-derived IL-13.Respiratory research · 2025Article
- Targeted peptide modification of mesenchymal stem cells enhances their therapeutic efficacy in the treatment of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2025Article
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
- Exploring the impact of mitochondrial-targeting anthelmintic agents with GLUT1 inhibitor BAY-876 on breast cancer cell metabolism.BMC cancer · 2024Article
- Review
- Article
- Niclosamide - encapsulated lipid nanoparticles for the reversal of pulmonary fibrosis.Materials today. Bio · 2024Article
- Improvement of idiopathic pulmonary fibrosis through a combination ofJournal of thoracic disease · 2024Article
- Understanding the molecular regulatory mechanisms of autophagy in lung disease pathogenesis.Frontiers in immunology · 2024Review
- The causal relationship between physical activity, sedentary time and idiopathic pulmonary fibrosis risk: a Mendelian randomization study.Respiratory research · 2023Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is an interstitial pneumonia characterized by chronic progressive fibrosis, ultimately leading to respiratory failure and early mortality. Although not fully explored, the major causative factors in IPF pathogenesis are dysregulated fibroblast proliferation and excessive accumulation of extracellular matrix (ECM) deposited by myofibroblasts differentiated from pulmonary fibroblasts. More signalling pathways, including the PI3K-Akt-mTOR and autophagy pathways, are involved in IPF pathogenesis. Niclosamide ethanolamine salt (NEN) is a highly effective multitarget small-molecule inhibitor reported in antitumor studies. Here, we reported that in an IPF animal model treated with NEN for 14 days, attractive relief of pulmonary function and hydroxyproline content were observed. To further explore, the therapeutic effect of NEN in IPF and pathological changes in bleomycin-challenged mouse lung sections were assessed. Additionally, the effects of NEN on abnormal proliferation and ECM production in IPF cell models established with TGF-β1-stimulated A549 cells or DHLF-IPF cells were studied. In nonclinical studies, NEN ameliorated lung function and histopathological changes in bleomycin-challenged mice, and the lung hydroxyproline content was significantly diminished with NEN treatment. In vitro, NEN inhibited PI3K-mTORC1 signalling and arrested the cell cycle to prevent uncontrolled fibroblast proliferation. Additionally, NEN inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT) and ECM accumulation via the mTORC1-4EBP1 axis. Furthermore, NEN-activated noncanonical autophagy resensitized fibroblasts to apoptosis. The above findings demonstrated the potential antifibrotic effect of NEN mediated via modulation of the PI3K-mTORC1 and autophagy pathways. These data provide strong evidence for a therapeutic role for NEN in IPF.
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What OpenQuestion holds
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.