ReviewFrontiers in medicine2025
Epithelial-mesenchymal transition in pulmonary fibrosis: molecular mechanisms and emerging therapeutic strategies.
Review in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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
9 citing papers in PubMed.
- Narrative Review of the Pathophysiology of Post-Infectious Bronchiolitis Obliterans.Biomolecules · 2026Review
- Senescent Alveolospheres: A Preliminary 3D Model for Exploring Epithelial Senescence and Pro-Fibrotic Signaling.International journal of molecular sciences · 2026Article
- Autophagy-epithelial-mesenchymal transition crosstalk in acute respiratory distress syndrome: Mechanistic insights and therapeutic perspectives (Review).Experimental and therapeutic medicine · 2026Review
- Plasminogen Activation System and Fibroblasts: Impact on Tissue Remodeling, Disease, and Organ Homeostasis.Inflammation · 2026Review
- Pulmonary Fibrosis Beyond the Lung: Adipose Tissue as a Systemic Modifier of Fibrotic Remodeling.Diagnostics (Basel, Switzerland) · 2026Review
- Cilostazol mitigates amiodarone-induced pulmonary toxicity and fibrosis by regulating the cAMP/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition in rats.Scientific reports · 2026Article
- Article
- Trained immunity in respiratory diseases: Mechanisms of action and intervention strategies.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Paclitaxel-eluting silicone airway stent with sustained drug release and potent anti-fibrotic activity.Frontiers in bioengineering and biotechnology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis is a progressive lung-scarring disease for which curative options remain limited. This review examines how epithelial-mesenchymal transition (EMT) contributes to fibrotic remodeling in subsets of pulmonary fibrosis (PF), delineates where the evidence is strongest, and highlights emerging therapeutic directions. PF encompasses idiopathic PF (IPF) and diverse non-IPF interstitial lung diseases driven by autoimmunity, exposures, or genetics, in which EMT involvement is variable. Recent laboratory and clinical work has been analyzed and the evidence grouped into four areas: well-known growth-factor signals; immune and inflammatory crosstalk; newer drivers such as iron-linked cell death, metabolic change and tissue stretch; and emerging medicines that temper these pathways, including licensed antifibrotics, experimental small molecules, natural compounds and RNA-based agents. Collectively, EMT emerges as a potentially reversible hub linking epithelial stress to scar formation, suggesting stage-specific combination strategies supported by single-cell profiling, lung organoids, and targeted delivery.
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Identifiers
What Socratic 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 Socratic graph.