ReviewThe Journal of pathology2003
Pathogenetic mechanisms in usual interstitial pneumonia/idiopathic pulmonary fibrosis.
Review in The Journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
101 citing papers in PubMed, 186 citations in OpenAlex.
- CD8+ T lymphocytes in lung tissue from patients with idiopathic pulmonary fibrosis.Respiratory research · 2005Trial
- Macropinocytosis inhibition attenuates profibrotic responses in lung fibroblasts and pulmonary fibrosis models.The Journal of clinical investigation · 2026Article
- Conditional BCL-2 Expression in Fibroblasts Promotes Persistent Pulmonary Fibrosis which is Reversible by Therapeutic BCL-2 Inhibition.Nature communications · 2026Article
- Potential of bone marrow mesenchymal stem cells in iodine-induced autoimmune thyroiditis therapy.European thyroid journal · 2025Article
- Cloned airway basal progenitor cells to repair fibrotic lung through re-epithelialization.Nature communications · 2025Article
- Inhibition of mTOR differently modulates planar and subepithelial fibrogenesis in human conjunctival fibroblasts.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025Article
- Network pharmacology-based approach to research the effects and mechanisms ofFrontiers in medicine · 2025Article
- Review
- Opposite effects of systemic and local conditional CD11c+ myeloid cell depletion during bleomycin-induced inflammation and fibrosis in mice.Immunity, inflammation and disease · 2024Article
- Article
- Anoctamin-1 is induced by TGF-β and contributes to lung myofibroblast differentiation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Transformation of macrophages into myofibroblasts in fibrosis-related diseases: emerging biological concepts and potential mechanism.Frontiers in immunology · 2024Review
- Geniposide ameliorates bleomycin-induced pulmonary fibrosis in mice by inhibiting TGF-β/Smad and p38MAPK signaling pathways.PloS one · 2024Article
- Anoctamin-1 is induced by TGF-beta and contributes to lung myofibroblast differentiation.bioRxiv : the preprint server for biology · 2023Article
- TGF-β Isoforms Affect the Planar and Subepithelial Fibrogenesis of Human Conjunctival Fibroblasts in Different Manners.Biomedicines · 2023Article
- Inhibition of Fatty Acid Amide Hydrolase (FAAH) Regulates NF-kb Pathways Reducing Bleomycin-Induced Chronic Lung Inflammation and Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- CC Chemokines in Idiopathic Pulmonary Fibrosis: Pathogenic Role and Therapeutic Potential.Biomolecules · 2023Review
- FGF-2 enhances fibrogenetic changes in TGF-β2 treated human conjunctival fibroblasts.Scientific reports · 2022Article
- Identification of three hub genes related to the prognosis of idiopathic pulmonary fibrosis using bioinformatics analysis.International journal of medical sciences · 2022Article
- Glycyrrhizic Acid Inhibits Core Fucosylation Modification Modulated EMT and Attenuates Bleomycin-Induced Pulmonary Fibrosis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
41 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 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive, usually fatal, form of interstitial lung disease characterized by failure of alveolar re-epithelialization, persistence of fibroblasts/myofibroblasts, deposition of extracellular matrix, and distortion of lung architecture which ultimately results in respiratory failure. Clinical IPF is associated with a histopathological pattern of usual interstitial pneumonia (UIP) on surgical lung biopsy. Therapy for this disease with glucocorticoids and other immunomodulatory agents is largely ineffective and recent trials of newer anti-fibrotic agents have been disappointing. While the inciting event(s) leading to the initiation of scar formation in UIP remain unknown, recent advances in our understanding of the mechanisms underlying both normal and aberrant wound healing have shed some light on pathogenetic mechanisms that may play significant roles in this disease. Unlike other fibrotic diseases of the lung, such as those associated with collagen vascular disease, occupational exposure, or chemotherapeutic agents, UIP is not associated with a significant inflammatory response; rather, dysregulated epithelial-mesenchymal interactions predominate. Identification of pathways crucial to fibrogenesis might offer potentially novel therapeutic targets to slow or halt the progression of IPF. This review focuses on evolving concepts of cellular and molecular mechanisms in the pathogenesis of UIP/IPF.
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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.