ReviewEuropean respiratory review : an official journal of the European Respiratory Society2012
Unravelling the progressive pathophysiology of idiopathic pulmonary fibrosis.
Review in European respiratory review : an official journal of the European Respiratory Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 147 citations in OpenAlex.
- Effect of statins on disease-related outcomes in patients with idiopathic pulmonary fibrosis.Thorax · 2017Trial
- Blood transcriptomic signatures distinguishEmerging microbes & infections · 2026Article
- Targeting fused in sarcoma (FUS): a novel antisense strategy for treating idiopathic pulmonary fibrosis.Signal transduction and targeted therapy · 2026Article
- MICA-129Met/Val as a therapeutic compass in idiopathic pulmonary fibrosis: prognosis and antifibrotic benefit.Frontiers in immunology · 2026Article
- FASN regulates CSE-induced apoptosis, oxidative stress and mitochondrial damage in type 2 alveolar epithelial cells by regulating NRF2 expression and nuclear translocation.Redox report : communications in free radical research · 2025Article
- Serum IgA levels and survival in patients with idiopathic pulmonary fibrosis: association with serum cytokine levels and peripheral monocyte counts.Journal of thoracic disease · 2025Article
- Evidence for a lipofibroblast-to-The European respiratory journal · 2025Article
- Targeting USP11 counteractsTheranostics · 2025Article
- Ferroptosis in idiopathic pulmonary fibrosis: mechanisms, impact, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Understanding myofibroblast origin in the fibrotic lung.Chinese medical journal pulmonary and critical care medicine · 2024Review
- Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges.Cell death discovery · 2024Review
- Role and targeting of the AGC kinase family in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2024Review
- Machine Learning and Single-Cell Analysis Identify Molecular Features of IPF-Associated Fibroblast Subtypes and Their Implications on IPF Prognosis.International journal of molecular sciences · 2023Article
- Exploring the Role of Biomarkers Associated with Alveolar Damage and Dysfunction in Idiopathic Pulmonary Fibrosis-A Systematic Review.Journal of personalized medicine · 2023Review
- Article
- Airway allergy causes alveolar macrophage death, profound alveolar disorganization and surfactant dysfunction.Frontiers in immunology · 2023Article
- Progress in Respiratory Gene Therapy.Human gene therapy · 2022Review
- Inflammation resolution in environmental pulmonary health and morbidity.Toxicology and applied pharmacology · 2022Review
- Article
- Review
3 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
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a life-threatening condition, with a median survival of <3 yrs. The pathophysiology is not fully understood, but chronic injury of alveolar epithelial type II cells (AECII) is considered key. In IPF, disturbed folding and processing of surfactant proteins and impaired DNA repair may represent underlying reasons for maladaptive endoplasmic reticulum stress responses, increased reactive oxygen species production and/or DNA damage. Excessive AECII apoptosis occurs, leading to permanently perturbed epithelial homeostasis. The role of secondary hits also becomes evident. These may aggravate the disease and result in increased epithelial turnover, exhausting the regenerative capacity of progenitors and disturbing epithelial-mesenchymal interactions. Fibroblast proliferation, transdifferentiation and matrix deposition may be mediated through various mechanisms including epithelial-mesenchymal transition, fibrocyte invasion or expansion of a local fibroblast population. Treatment modalities aiming to attenuate epithelial injury are currently in early pre-clinical development and may reach the clinical arena in only a few years. Meanwhile, novel drugs acting on highly activated fibroblasts such as pirfenidone, an anti-fibrotic drug authorised for IPF in the European Union, or BIBF 1120, a novel triple-kinase inhibitor (blocking vascular endothelial growth factor, platelet-derived growth factor and fibroblast growth factor) currently under clinical investigation, seem to attenuate the progression of IPF.
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.