ArticleJournal of lung health and diseases2019
Epithelial-mesenchymal transition contributes to pulmonary fibrosis via aberrant epithelial/fibroblastic cross-talk.
Article in Journal of lung health and diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Protective effects and mechanism of curcumin in animal models of pulmonary fibrosis: a preclinical systematic review and meta-analysis.Frontiers in pharmacology · 2023Pooled it
- A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026Review
- Sinigrin Mitigates Pulmonary Inflammation and Fibrosis Partly through Adenosine Monophosphate-Activated Protein Kinase (AMPK) Signaling.ACS pharmacology & translational science · 2026Article
- mExperimental and therapeutic medicine · 2026Review
- Molecular insights into the anti-inflammatory and antifibrotic effects of licorice-ginger decoction in experimental models of inflammatory arthritis-associated lung fibrosis.Immunology and cell biology · 2026Article
- Autophagy-epithelial-mesenchymal transition crosstalk in acute respiratory distress syndrome: Mechanistic insights and therapeutic perspectives (Review).Experimental and therapeutic medicine · 2026Review
- Research trends and hot topics of radiation-induced pulmonary fibrosis: a bibliometric analysis and visualization study from 2015 to 2025.Journal of thoracic disease · 2026Article
- Plasminogen Activation System and Fibroblasts: Impact on Tissue Remodeling, Disease, and Organ Homeostasis.Inflammation · 2026Review
- Deficiency of GCN5 exacerbates pulmonary fibrosis by disrupting the LKB1-AMPK pathway.Cell communication and signaling : CCS · 2026Article
- Therapeutic Potential of Lentiviral miR-200a Mimics in Regulating Fibrinolysis and EMT Markers During Pulmonary Fibrosis.FASEB bioAdvances · 2026Article
- STING-STAT3-SOX18 Axis Drives EndMT and Epigenetic Reprogramming in SAVI Lung Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Viral Pathogens and Pulmonary Fibrosis: EMT-Driven Mechanisms and Insights From Traditional Chinese Medicine.Reviews in medical virology · 2026Review
- Dahuang Zhechong pill alleviates pulmonary fibrosis by inhibiting apoptosis and epithelial-mesenchymal transition of type II alveolar epithelial cellsJournal of traditional and complementary medicine · 2026Article
- Most Promising Emerging Therapies for Pulmonary Fibrosis: Targeting Novel Pathways.Biomedicines · 2026Review
- An hiPSC-derived multi-lineage lung model exhibiting proximal-distal epithelial features for modeling pulmonary fibrosis.Frontiers in cell and developmental biology · 2026Article
- MMP-7 as a non-invasive biomarker in interstitial lung diseases and other chronic respiratory diseases: a narrative review.Frontiers in medicine · 2026Review
- Pulmonary fibrosis in post-COVID-19: epithelial-mesenchymal transition as a key mechanism and target for therapy.Inflammopharmacology · 2026Review
- Alpha-1-antichymotrypsin: a potential inducer for epithelial-mesenchymal transition in lupus nephritis.Open life sciences · 2026Article
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- SARS-CoV-2-encoded miR-nsp3-3p promotes pulmonary fibrosis by inhibiting expression of ALCAM.Virologica Sinica · 2025Article
32 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic interstitial lung disease. Median survival is only 3 years, and treatment options are limited. IPF is thought to be a result of a combination of genetic and environmental factors with repetitive micro-injuries to alveolar epithelial cells playing a central role. IPF is characterised by aberrant extra cellular matrix (ECM) deposition by activated myofibroblasts. Epithelial-mesenchymal transition (EMT) is a process where polarised epithelial cells undergo molecular changes allowing them to gain a mesenchymal phenotype, with a subsequent enhanced ability to produce ECM components and increased migration and/or invasion. The source of myofibroblasts in IPF has been debated for many years, and EMT has been proposed as a source of these cells. However, lineage tracing in transgenic mice suggests the contribution of epithelial cells, which have undergone EMT, to the fibroblast population may be negligible. Instead, recent findings suggest that alveolar epithelial type II (ATII) cells undergoing EMT promote a pro-fibrotic microenvironment through paracrine signalling activating local fibroblasts. This review paper explores the contribution of ATII cells, which have undergone EMT, in the context of pulmonary fibrosis.
Identifiers
31032489PMC6485666W2945050016What 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.