ReviewJournal of clinical medicine2019
Mucins as a New Frontier in Pulmonary Fibrosis.
Review in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed.
- Investigation of telomere related gene mutations in idiopathic pulmonary fibrosis.Molecular biology reports · 2020Trial
- Somatic mutation analysis of mucin genes and pathways in idiopathic pulmonary fibrosis.American journal of respiratory and critical care medicine · 2026Article
- Persistent loss of membrane-associated MUC4 reprograms physiological functions in corneal epithelial cells via MAPK-dependent cascade.Scientific reports · 2026Article
- Circulating biomarkers in subjects with progressive pulmonary fibrosis: data from the INBUILD trial.ERJ open research · 2026Article
- Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025Review
- Hypoxia-inducible factor-1α promotes tubulointerstitial fibrosis via the upregulation ofRenal failure · 2025Article
- MUC1 in the upper-lower airway inflammatory continuum: an endotype-centered perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- The predictive value of MUC5AC levels in the sputum of children withMicrobiology spectrum · 2025Article
- Deciphering the interplay: circulating cell-free DNA, signaling pathways, and disease progression in idiopathic pulmonary fibrosis.3 Biotech · 2025Review
- The multifaceted roles of mucins family in lung cancer: from prognostic biomarkers to promising targets.Frontiers in immunology · 2025Review
- Validation of the KL6 Method on the G600II Analyser (Lumipulse) for Clinical Use in Interstitial Lung Disease.EJIFCC · 2024Article
- Transcriptomics using lung resection material to advance our understanding of COPD and idiopathic pulmonary fibrosis pathogenesis.ERJ open research · 2024Article
- Genetic Underpinnings of Pulmonary Fibrosis: An Overview.Cardiovascular & hematological agents in medicinal chemistry · 2024Review
- Clonal Somatic Mutations in Chronic Lung Diseases Are Associated with Reduced Lung Function.American journal of respiratory and critical care medicine · 2023Article
- Mucin glycans and their degradation by gut microbiota.Glycoconjugate journal · 2023Review
- Identification of RAC1 in promoting brain metastasis of lung adenocarcinoma using single-cell transcriptome sequencing.Cell death & disease · 2023Article
- Spatial metabolomics reveals glycogen as an actionable target for pulmonary fibrosis.Nature communications · 2023Article
- Matrix metalloproteinase-7 is increased in lung bases but not apices in idiopathic pulmonary fibrosis.ERJ open research · 2022Article
- Smoking-associated Downregulation of FILIP1L Enhances Lung Adenocarcinoma Progression Through Mucin Production, Inflammation, and Fibrosis.Cancer research communications · 2022Article
- JiangShi(): a widely distributed Mucin-like protein essential for Drosophila development.G3 (Bethesda, Md.) · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is the most common idiopathic interstitial pulmonary disease with a median survival of 3-5 years after diagnosis. Recent evidence identifies mucins as key effectors in cell growth and tissue remodeling processes compatible with the processes observed in IPF. Mucins are classified in two groups depending on whether they are secreted (secreted mucins) or tethered to cell membranes (transmembrane mucins). Secreted mucins (MUC2, MUC5AC, MUC5B, MUC6-8 and MUC19) are released to the extracellular medium and recent evidence has shown that a promoter polymorphism in the secreted mucin MUC5B is associated with IPF risk. Otherwise, transmembrane mucins (MUC1, MUC3, MUC4, MUC12-17 and MUC20) have a receptor-like structure, sensing the external environment and activating intracellular signal transduction pathways essential for mucosal maintenance and damage repair. In this context, the extracellular domain can be released to the external environment by metalloproteinase action, increased in IPF, thus activating fibrotic processes. For example, several studies have reported increased serum extracellular secreted KL6/MUC1 during IPF acute exacerbation. Moreover, MUC1 and MUC4 overexpression in the main IPF cells has been observed. In this review we summarize the current knowledge of mucins as promising druggable targets for IPF.
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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.