ArticleThe American journal of pathology2003
Persistent down-regulation of Fli1, a suppressor of collagen transcription, in fibrotic scleroderma skin.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 167 citations in OpenAlex.
- Fli1 represses transcription of the human α2(I) collagen gene by recruitment of the HDAC1/p300 complex.PloS one · 2013Trial
- Pumping Up Dermatologic Drug Reformulation: A Review of How Proton Pump Inhibitors May Revolutionize Scleroderma Treatment.The Journal of clinical and aesthetic dermatology · 2026Review
- Role of Transcription Factor Fli-1 in Inflammation and Autoimmune Diseases.Biomolecules · 2025Review
- Virus-Induced MicroRNA Modulation and Systemic Sclerosis Disease.Biomedicines · 2024Review
- The Pathogenesis of Systemic Sclerosis: The Origin of Fibrosis and Interlink with Vasculopathy and Autoimmunity.International journal of molecular sciences · 2023Review
- Development and characterization of an ETV1 rabbit monoclonal antibody for the immunohistochemical detection of ETV1 expression in cancer tissue specimens.Journal of immunological methods · 2023Article
- Fli1 and Tissue Fibrosis in Various Diseases.International journal of molecular sciences · 2023Review
- Suppression of Fli-1 protects against pericyte loss and cognitive deficits in Alzheimer's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Endothelial CCR6 expression due to FLI1 deficiency contributes to vasculopathy associated with systemic sclerosis.Arthritis research & therapy · 2021Article
- Camptothecin and Topotecan, Inhibitors of Transcription Factor Fli-1 and Topoisomerase, Markedly Ameliorate Lupus Nephritis in (NZB × NZW)F1 Mice and Reduce the Production of Inflammatory Mediators in Human Renal Cells.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Fli1 deficiency suppresses RALDH1 activity of dermal dendritic cells and related induction of regulatory T cells: a possible role in scleroderma.Arthritis research & therapy · 2021Article
- FLI1 and ERG protein degradation is regulated via Cathepsin B lysosomal pathway in human dermal microvascular endothelial cells.Microcirculation (New York, N.Y. : 1994) · 2021Article
- A Flowable Placental Formulation Prevents Bleomycin-Induced Dermal Fibrosis in Aged Mice.International journal of molecular sciences · 2020Article
- Therapeutic molecular targets of SSc-ILD.Journal of scleroderma and related disorders · 2020Article
- Fli1 Downregulation in Scleroderma Myeloid Cells Has Profibrotic and Proinflammatory Effects.Frontiers in immunology · 2020Article
- Epigenetic Control of Scleroderma: Current Knowledge and Future Perspectives.Current rheumatology reports · 2019Review
- Active roles of dysfunctional vascular endothelium in fibrosis and cancer.Journal of biomedical science · 2019Review
- Cyclophosphamide Pulse Therapy Normalizes Vascular Abnormalities in a Mouse Model of Systemic Sclerosis Vasculopathy.The Journal of investigative dermatology · 2019Article
- What can we learn fromJournal of scleroderma and related disorders · 2018Review
- The Activation of Human Dermal Microvascular Cells by Poly(I:C), Lipopolysaccharide, Imiquimod, and ODN2395 Is Mediated by the Fli1/FOXO3A Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The molecular and cellular mechanisms that maintain proper collagen homeostasis in healthy human skin and are responsible for the dysregulated collagen synthesis in scleroderma remain primarily unknown. This study demonstrates that Fli1 is a physiological negative regulator of collagen gene expression in dermal fibroblasts in vitro and in human skin in vivo. This conclusion is supported by the analyses of mouse embryonic fibroblasts from Fli1(-/-), Fli1(+/-), and Fli1(+/+) mice. In cultured human and mouse fibroblasts Fli1 expression levels are inversely correlated with the collagen type I expression levels. These in vitro observations were validated in vivo. In healthy human skin Fli1 protein is expressed in fibroblasts and endothelial cells. Significantly, absence of Fli1 expression in individual fibroblasts correlates with elevated collagen synthesis. In contrast to healthy skin, Fli1 protein is consistently absent from fibroblasts and significantly reduced in endothelial cells in clinically involved scleroderma skin, which correlates with enhanced collagen synthesis in systemic sclerosis skin. This study supports the role of Fli1 as a suppressor of collagen transcription in human skin in vivo. Persistent down-regulation of Fli1 in scleroderma fibroblasts in vivo may directly contribute to uncontrolled matrix deposition in scleroderma skin.
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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.