ReviewBritish journal of pharmacology2011
Novel therapeutic approaches for pulmonary fibrosis.
Review in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
87 citing papers in PubMed, 1 synthesis or guideline pooled it, 201 citations in OpenAlex.
- The pattern of human papillomavirus infection and genotypes among Nigerian women from 1999 to 2019: a systematic review.Annals of medicine · 2021Pooled it
- Fibronectin's tensional state as a mechanical signature of fibrotic extracellular matrix in idiopathic pulmonary fibrosis models.Matrix biology plus · 2026Article
- Andrographolide Modulates Fibrogenic and Oxidative Stress Responses in Human Lung Fibroblasts.The Kaohsiung journal of medical sciences · 2026Article
- Article
- p53-miR-34a feedback in lung fibroblasts regulates antifibrotic effects of CSP7, nintedanib, and pirfenidone.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Targeting JNK1/2 and P38 Mitogen-Activated Protein Kinases With Pazopanib Mitigates Bleomycin-Induced Lung Fibrosis.Archiv der Pharmazie · 2025Article
- Article
- Pirfenidone and Nintedanib in Pulmonary Fibrosis: Lights and Shadows.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Glutaminolysis regulates endometrial fibrosis in intrauterine adhesion via modulating mitochondrial function.Biological research · 2024Article
- Betulin andHeliyon · 2023Article
- A roadmap for developing and engineeringBiophysics reviews · 2023Review
- Bioengineering and Clinical Translation of Human Lung and its Components.Advanced biology · 2023Review
- Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022Review
- Specific epigenetic regulators serve as potential therapeutic targets in idiopathic pulmonary fibrosis.Heliyon · 2022Review
- Inhibition of nuclear factor κB in the lungs protect bleomycin-induced lung fibrosis in mice.Molecular biology reports · 2022Article
- Candidate Role for Toll-like Receptor 3 L412F Polymorphism and Infection in Acute Exacerbation of Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2022Article
- Study on the Mechanism of Astragalus Polysaccharide in Treating Pulmonary Fibrosis Based on "Drug-Target-Pathway" Network.Frontiers in pharmacology · 2022Article
- Combined transcriptomic and lipidomic analysis of D-4F ameliorating bleomycin-induced pulmonary fibrosis.Annals of translational medicine · 2021Article
- Kurarinone Attenuates BLM-Induced Pulmonary Fibrosis via Inhibiting TGF-β Signaling Pathways.International journal of molecular sciences · 2021Article
- VEGFR1-tyrosine kinase signaling in pulmonary fibrosis.Inflammation and regeneration · 2021Review
27 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary fibrosis represents the end stage of a number of heterogeneous conditions and is, to a greater or lesser degree, the hallmark of the interstitial lung diseases. It is characterized by the excessive deposition of extracellular matrix proteins within the pulmonary interstitium leading to the obliteration of functional alveolar units and in many cases, respiratory failure. While a small number of interstitial lung diseases have known aetiologies, most are idiopathic in nature, and of these, idiopathic pulmonary fibrosis is the most common and carries with it an appalling prognosis - median survival from the time of diagnosis is less than 3 years. This reflects the lack of any effective therapy to modify the course of the disease, which in turn is indicative of our incomplete understanding of the pathogenesis of this condition. Current prevailing hypotheses focus on dysregulated epithelial-mesenchymal interactions promoting a cycle of continued epithelial cell injury and fibroblast activation leading to progressive fibrosis. However, it is likely that multiple abnormalities in a myriad of biological pathways affecting inflammation and wound repair - including matrix regulation, epithelial reconstitution, the coagulation cascade, neovascularization and antioxidant pathways - modulate this defective crosstalk and promote fibrogenesis. This review aims to offer a pathogenetic rationale behind current therapies, briefly outlining previous and ongoing clinical trials, but will focus on recent and exciting advancements in our understanding of the pathogenesis of idiopathic pulmonary fibrosis, which may ultimately lead to the development of novel and effective therapeutic interventions for this devastating condition.
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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.