ArticleFibrogenesis & tissue repair2012
Fibrocytes and the pathogenesis of diffuse parenchymal lung disease.
Article in Fibrogenesis & tissue repair, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Pathogenesis and current status of the treatment of lung cancer associated with idiopathic pulmonary fibrosis.Respiratory research · 2025Review
- The Novel Regulatory Role of the lncRNA-miRNA-mRNA Axis in Chronic Inflammatory Airway Diseases.Frontiers in molecular biosciences · 2022Review
- Role of fibrocytes and endothelial progenitor cells among low-differentiated CD34+ cells in the progression of lung sarcoidosis.BMC pulmonary medicine · 2020Article
- Circulating fibrocytes as prognostic biomarkers of autoimmune interstitial lung disease.ERJ open research · 2020Article
- Asiaticoside might attenuate bleomycin-induced pulmonary fibrosis by activating cAMP and Rap1 signalling pathway assisted by A2AR.Journal of cellular and molecular medicine · 2020Article
- Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets.International journal of molecular sciences · 2019Review
- Altered pattern of monocyte differentiation and monocyte-derived TGF-β1 in severe asthma.Scientific reports · 2018Article
- Myeloproliferative leukemia protein activation directly induces fibrocyte differentiation to cause myelofibrosis.Leukemia · 2017Article
- Circulating fibrocytes as biomarkers of impaired lung function in adults with sickle cell disease.Blood advances · 2017Article
- Role of neoplastic monocyte-derived fibrocytes in primary myelofibrosis.The Journal of experimental medicine · 2016Article
- Circulating fibrocytes as biomarker of prognosis in Hermansky-Pudlak syndrome.American journal of respiratory and critical care medicine · 2014Article
- Bone marrow-derived stromal cells are invasive and hyperproliferative and alter transforming growth factor-α-induced pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2014Article
- Fibrocytes in pulmonary fibrosis: a brief synopsis.European respiratory review : an official journal of the European Respiratory Society · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fibrosis is fundamental to the pathogenesis of many chronic lung diseases, including some lung infections, airway diseases such as bronchiectasis and asthma, and most of the diffuse parenchymal lung diseases. Idiopathic pulmonary fibrosis, the prototypical fibrotic lung disease, is amongst the most common diffuse parenchymal lung diseases and is characterized by progressive decline in lung function and premature death from respiratory failure. The clinical management of patients with this illness is hampered by our current inability to predict clinical deterioration and lack of an effective therapy. Fibrocytes are a population of bone marrow-derived circulating progenitor cells that home to injured tissues and differentiate into fibroblasts and myofibroblasts, thus contributing to scar formation. We summarize the evidence supporting the role of these cells in the pathogenesis of fibrotic lung diseases.
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.