ReviewDrugs2004
Idiopathic pulmonary fibrosis: pathogenesis and therapeutic approaches.
Review in Drugs, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05353556 (Effects of Home-based Inspiratory Muscle Training in Patients With Idiopathic Pulmonary Fibrosis), which is not on this map. Cited by 90 papers, 1 of them a synthesis that pooled it.
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.
Effects of Home-based Inspiratory Muscle Training in Patients With Idiopathic Pulmonary Fibrosis
Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.
- Meta-analysis of transcriptomic responses as a means to identify pulmonary disease outcomes for engineered nanomaterials.Particle and fibre toxicology · 2016Pooled it
- Activation of the impaired NAMPT/SIRT7/SOD2 axis restores alveolar progenitor cell renewal in idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2026Article
- Senescence intensifies bleomycin-induced injury in idiopathic pulmonary fibrosis lung epithelial cells.ERJ open research · 2026Article
- Mitophagy promotes lung repair and regeneration by restoring epithelial metabolic fitness.Nature communications · 2026Article
- High matrix stiffness promotes senescence of type II alveolar epithelial cells by lysosomal degradation of lamin A/C in pulmonary fibrosis.Respiratory research · 2025Article
- Lung Cancer and Interstitial Lung Diseases.Cancers · 2024Review
- Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges.Cell death discovery · 2024Review
- The aging lung: microenvironment, mechanisms, and diseases.Frontiers in immunology · 2024Review
- A roadmap for developing and engineeringBiophysics reviews · 2023Review
- Modeling of Respiratory Diseases Evolving with Fibrosis from Organoids Derived from Human Pluripotent Stem Cells.International journal of molecular sciences · 2023Review
- Coal dust nanoparticles induced pulmonary fibrosis by promoting inflammation and epithelial-mesenchymal transition via the NF-κB/NLRP3 pathway driven by IGF1/ROS-mediated AKT/GSK3β signals.Cell death discovery · 2022Article
- Role of MicroRNAs in Signaling Pathways Associated with the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Focus on Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2022Review
- ASK1ng to Delay the Progression of Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Gas6 Ameliorates Inflammatory Response and Apoptosis in Bleomycin-Induced Acute Lung Injury.Biomedicines · 2021Article
- The development of HEC-866 and its analogues for the treatment of idiopathic pulmonary fibrosis.RSC medicinal chemistry · 2021Article
- Article
- Captopril reduces lung inflammation and accelerated senescence in response to thoracic radiation in mice.Journal of radiation research · 2021Article
- Lipid Metabolism Profiles in Rheumatic Diseases.Frontiers in pharmacology · 2021Review
- HGF-Modified Dental Pulp Stem Cells Mitigate the Inflammatory and Fibrotic Responses in Paraquat-Induced Acute Respiratory Distress Syndrome.Stem cells international · 2021Article
- The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis.Life (Basel, Switzerland) · 2020Review
30 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 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF), also termed cryptogenic fibrosing alveolitis, is a clinicopathological syndrome characterised by cough, exertional dyspneoa, basilar crackles, a restrictive defect on pulmonary function tests, honeycombing on high-resolution, thin-section computed tomographic scans and the histological diagnosis of usual interstitial pneumonia on lung biopsy. The course is usually indolent but inexorable. Most patients die of progressive respiratory failure within 3-8 years of the onset of symptoms. Current therapies are of unproven benefit. Although the pathogenesis of IPF has not been elucidated, early concepts focused on lung injury leading to a cycle of chronic alveolar inflammation eventuating in fibrosis and destruction of the lung architecture. Anti-inflammatory therapies employing corticosteroids or immunosuppressive or cytotoxic agents have been disappointing. More recent hypotheses acknowledge that sequential alveolar epithelial cell injury is likely to be a key event in the pathogenesis of IPF, but the cardinal event is an aberrant host response to wound healing. In this context, abnormal epithelial-mesenchymal interactions, altered fibroblast phenotypes, exaggerated fibroblast proliferation, and excessive deposition of collagen and extracellular matrix are pivotal to the fibrotic process. Several clinical trials are currently underway or in the planning stages, and include drugs such as interferon-gamma 1b, pirfenidone, acetylcysteine, etanercept (a tumor necrosis factor-alpha antagonist), bosentan (an endothelin-1 receptor antagonist) and zileuton (a 5-lypoxygenase inhibitor). Future therapeutic strategies should be focused on alveolar epithelial cells aimed at enhancing re-epithelialisation and on fibroblastic/myofibroblastic foci, which play an essential role in the development of IPF. Stem cell progenitors of the alveolar epithelial cells and genetic and epigenetic therapies are attractive future approaches for this and other fibrotic lung disorders.
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.