ArticleThe American journal of pathology1986
Intraluminal fibrosis in interstitial lung disorders.
Article in The American journal of pathology, 1986. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed.
- The Plastic Interplay between Lung Regeneration Phenomena and Fibrotic Evolution: Current Challenges and Novel Therapeutic Perspectives.International journal of molecular sciences · 2023Review
- Histologic Characteristics and Clinical Courses of Primary Viral Pneumonia Other than COVID-19.Internal medicine (Tokyo, Japan) · 2023Article
- Hypoxia enhances IPF mesenchymal progenitor cell fibrogenicity via the lactate/GPR81/HIF1α pathway.JCI insight · 2023Article
- Mechanoresponsive regulation of fibroblast-to-myofibroblast transition in three-dimensional tissue analogues: mechanical strain amplitude dependency of fibrosis.Scientific reports · 2022Article
- Article
- Review
- Review
- Inhibitors of the Autotaxin-Lysophosphatidic Acid Axis and Their Potential in the Treatment of Interstitial Lung Disease: Current Perspectives.Clinical pharmacology : advances and applications · 2020Review
- Is Progression of Pulmonary Fibrosis due to Ventilation-induced Lung Injury?American journal of respiratory and critical care medicine · 2019Review
- Vimentin intermediate filament assembly regulates fibroblast invasion in fibrogenic lung injury.JCI insight · 2019Article
- Idiopathic Pulmonary Fibrosis (IPF): An Overview.Journal of clinical medicine · 2018Review
- Fibrogenic Lung Injury Induces Non-Cell-Autonomous Fibroblast Invasion.American journal of respiratory cell and molecular biology · 2016Article
- Profibrotic role of WNT10A via TGF-β signaling in idiopathic pulmonary fibrosis.Respiratory research · 2016Article
- Reduced FoxO3a expression causes low autophagy in idiopathic pulmonary fibrosis fibroblasts on collagen matrices.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Pathologic Regulation of Collagen I by an Aberrant Protein Phosphatase 2A/Histone Deacetylase C4/MicroRNA-29 Signal Axis in Idiopathic Pulmonary Fibrosis Fibroblasts.American journal of respiratory cell and molecular biology · 2015Article
- Lymphangiogenesis and Lesion Heterogeneity in Interstitial Lung Diseases.Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2015Review
- Pneumocyte injury and ubiquitin-positive pneumocytes in interstitial lung diseases.Histopathology · 2015Review
- New therapeutic targets in idiopathic pulmonary fibrosis. Aiming to rein in runaway wound-healing responses.American journal of respiratory and critical care medicine · 2014Review
- MicroRNA-96 inhibits FoxO3a function in IPF fibroblasts on type I collagen matrix.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- miR-210 promotes IPF fibroblast proliferation in response to hypoxia.American journal of physiology. Lung cellular and molecular physiology · 2014Article
8 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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histopathologic and ultrastructural features of intraluminal organizing and fibrotic changes were studied in open lung biopsies and autopsy specimens from 373 patients with interstitial lung disorders, including hypersensitivity pneumonitis (n = 44), idiopathic pulmonary fibrosis (n = 92), collagen-vascular diseases (n = 20), chronic eosinophilic pneumonia (n = 10), pulmonary histiocytosis X (n-90), pulmonary sarcoidosis (n = 62), pneumoconioses (n = 25), Legionnaire's disease (n = 5), drug- and toxin-induced pneumonitis (n = 4), radiation-induced pneumonitis (n = 2), lymphangioleiomyomatosis (n = 11), and chronic organizing pneumonia of unknown cause (n = 8). Three patterns of intraluminal organization and fibrosis were recognized: 1) intraluminal buds, which partially filled the alveoli, alveolar ducts and/or distal bronchioles; 2) obliterative changes, in which loose connective tissue masses obliterated the lumens of alveoli, alveolar ducts or distal bronchioles, and 3) mural incorporation of previously intraluminal connective tissue masses, which fused with alveolar, alveolar ductal, or bronchiolar structures and frequently became reepithelialized. All three patterns had common morphologic features, suggesting that, regardless of their severity, they resulted from a common pathogenetic mechanism, ie, the migration of activated connective tissue cells, through defects in the epithelial lining and its basement membrane, from the interstitial into the intraluminal compartment. Intraluminal buds were observed most frequently in hypersensitivity pneumonitis, chronic eosinophilic pneumonia, and organizing pneumonia of unknown cause. Mural incorporation and, to a lesser extent, obliterative changes were observed in most interstitial disorders and were very prominent in idiopathic pulmonary fibrosis. Mural incorporation and obliterative changes play an important role in pulmonary remodeling, especially when several adjacent alveoli and/or other air spaces are involved. Under these circumstances, intraluminal organization can mediate the fusion of adjacent alveolar structures by intraluminal connective tissue.
Indexed as
Identifiers
3953768PMC1888228What 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.