ReviewThe Lancet. Respiratory medicine2018
Time for a change: is idiopathic pulmonary fibrosis still idiopathic and only fibrotic?
Review in The Lancet. Respiratory medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06327360 (Between Beliefs and Expectations in Pulmonary Fibrosis), which is not on this map. Cited by 101 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Between Beliefs and Expectations in Pulmonary Fibrosis: a Prospective Cohort Study With Mixed Methods.
Who cites it
101 citing papers in PubMed, 190 citations in OpenAlex.
- A fibroblast-dependent TGF-β1/sFRP2 noncanonical Wnt signaling axis promotes epithelial metaplasia in idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2024Trial
- Safety, tolerability, pharmacokinetic/pharmacodynamic characteristics of bersiporocin, a novel prolyl-tRNA synthetase inhibitor, in healthy subjects.Clinical and translational science · 2023Trial
- Telomere dysfunction and mucociliary impairment drive idiopathic pulmonary fibrosis susceptibility: insights from a Sardinian whole-exome study.BMJ open respiratory research · 2026Article
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Recent advances in pulmonary fibrosis: from lung surfactant to the immune connection.Respiratory research · 2026Review
- Microplastics as environmental modifiers of lung disease.EMBO molecular medicine · 2026Review
- Neural regulatory networks: challenges and opportunities in the treatment of psoriasis.Frontiers in immunology · 2026Review
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- Article
- N-phenylquinazolin-4-amine-based EGFR TKIs suppress pulmonary fibrosis by modulating the EGFR/ERBB3 axis in epithelial-macrophage interaction.Communications biology · 2025Article
- Metabolomic profiling reveals distinct lipid signatures in progressive versus stable fibrotic lung disease.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Pharmacologic inhibition of IRE1α-dependent decay protects alveolar epithelial identity and prevents pulmonary fibrosis in mice.The Journal of clinical investigation · 2025Article
- The Role of Particle Inhalation in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2025Review
- Inhibition of Circadian Rhythm GeneEnvironment & health (Washington, D.C.) · 2025Article
- Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models.Nature communications · 2025Article
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- Uridine alleviates the aging of alveolar epithelial cells in idiopathic pulmonary fibrosis through the Keap1-Nrf2 signaling pathway.Scientific reports · 2025Article
- Review
- Immune mechanisms and novel therapies for idiopathic pulmonary fibrosis.Pharmaceutical science advances · 2024Review
- Pulmonary fibroblast-specific delivery of siRNA exploiting exosomes-based nanoscaffolds for IPF treatment.Asian journal of pharmaceutical sciences · 2024Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
15 authors at 12 institutions in 6 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible, and typically fatal lung disease characterised by subpleural fibrosis, subepithelial fibroblast foci, and microscopic honeycombing. Although understanding of the pathogenic mechanisms continues to evolve, evidence indicates that distal airway and alveolar epithelial cells are central drivers of the disease. In this Viewpoint, we review the history of naming and classifications used to define the disease now referred to as IPF, in the context of understanding the clinical presentation, causes, and pathogenesis of the disease. We aim to generate discussion on whether, given the substantial progress made in understanding the clinical, genetic, cellular, and molecular mechanisms involved in the development of IPF, a change of name should be considered. To initiate this discussion, we offer new suggestions to update the name of this disease and new approaches to classify all forms of pulmonary fibrosis.
Indexed as
Identifiers
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.