ArticlePulmonary medicine2011
Relative Roles of TGF-β and IGFBP-5 in Idiopathic Pulmonary Fibrosis.
Article in Pulmonary medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 25 citations in OpenAlex.
- Deciphering the role of IGFBP5 in delaying fibrosis and sarcopenia in aging skeletal muscle: therapeutic implications and molecular mechanisms.Frontiers in pharmacology · 2025Article
- Expression of insulin-like growth factor binding protein 5 in the vaginal wall tissues of older women with pelvic organ prolapse.Scientific reports · 2024Article
- Development of Galectin-3 Targeting Drugs for Therapeutic Applications in Various Diseases.International journal of molecular sciences · 2023Review
- Loss of IGFBP2 mediates alveolar type 2 cell senescence and promotes lung fibrosis.Cell reports. Medicine · 2023Article
- Molecular mechanisms of COVID-19-induced pulmonary fibrosis and epithelial-mesenchymal transition.Frontiers in pharmacology · 2023Review
- Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9.International journal of molecular sciences · 2022Review
- Elevated Serum IGFBP-2 and CTGF Levels Are Associated with Disease Activity in Patients with Dermatomyositis.Disease markers · 2022Article
- Identification of Impacted Pathways and Transcriptomic Markers as Potential Mediators of Pulmonary Fibrosis in Transgenic Mice Expressing Human IGFBP5.International journal of molecular sciences · 2021Article
- Emerging drug delivery strategies for idiopathic pulmonary fibrosis treatment.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2021Review
- Integrative analysis of transcriptional profile reveals LINC00052 as a suppressor of breast cancer cell migration.Cancer biomarkers : section A of Disease markers · 2021Article
- Gamma Tocotrienol Protects Mice From Targeted Thoracic Radiation Injury.Frontiers in pharmacology · 2020Article
- Autoantibodies in lung transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2020Review
- Intracellular Heat Shock Protein 70 Deficiency in Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2019Article
- Insulin-Like Growth Factor Binding Protein 5-A Probable Target of Kidney Renal Papillary Renal Cell Carcinoma.BioMed research international · 2019Article
- TGF-β signaling in the kidney: profibrotic and protective effects.American journal of physiology. Renal physiology · 2016Review
- Uridine supplementation exerts anti-inflammatory and anti-fibrotic effects in an animal model of pulmonary fibrosis.Respiratory research · 2015Article
- Systems analysis of transcriptional data provides insights into muscle's biological response to botulinum toxin.Muscle & nerve · 2014Article
- Insulin-like growth factor binding proteins-3 and -5: central mediators of fibrosis and promising new therapeutic targets.The open rheumatology journal · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although most evident in the skin, the process of scarring, or fibrosis, occurs in all major organs because of impaired epithelial self-renewal. No current therapy exists for Idiopathic pulmonary fibrosis. The major profibrotic factor is TGF-β1 and developing inhibitors is an area of active research. Recently, IGFBP-5 has also been identified as a profibrotic factor, and studies suggest that, while both TGF-β1 and IGFBP-5 activate mesenchymal cells to increase collagen and fibronectin production, their effects on epithelial cells are distinct. TGF-β1 induces cell death and/or EMT in the epithelial cells, exacerbating the disruption of tissue architecture. In contrast, IGFBP-5 induces epithelial cell spreading over collagen or fibronectin matrices, increases secretion of laminin, the epithelial basement membrane, and enhances the survival of epithelial cells in nutrient-poor conditions, as exists in scar tissue. Thus, IGFBP-5 may enhance repair and may be an important target for antifibrotic therapies.
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.