ReviewCurrent rheumatology reports2005
Scleroderma, fibroblasts, signaling, and excessive extracellular matrix.
Review in Current rheumatology reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 46 citations in OpenAlex.
- Assessment of skin fibrosis in a murine model of systemic sclerosis with multifunctional optical coherence tomography.Journal of biomedical optics · 2025Article
- scPanel: a tool for automatic identification of sparse gene panels for generalizable patient classification using scRNA-seq datasets.Briefings in bioinformatics · 2024Article
- Could Gas6/TAM Axis Provide Valuable Insights into the Pathogenesis of Systemic Sclerosis?Current issues in molecular biology · 2024Review
- Delivery technologies for therapeutic targeting of fibronectin in autoimmunity and fibrosis applications.Advanced drug delivery reviews · 2024Review
- Fibroblast activation protein: Pivoting cancer/chemotherapeutic insight towards heart failure.Biochemical pharmacology · 2024Review
- Release of TGF-βPharmaceutics · 2023Article
- Lung-kidney interactions and their role in chronic kidney disease-associated pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2022Review
- Collagen Structure-Function Mapping Informs Applications for Regenerative Medicine.Bioengineering (Basel, Switzerland) · 2020Review
- Integrated, multicohort analysis of systemic sclerosis identifies robust transcriptional signature of disease severity.JCI insight · 2016Article
- Vasculopathy in scleroderma.Seminars in immunopathology · 2015Review
- Cytokines in the immunopathology of systemic sclerosis.Seminars in immunopathology · 2015Review
- Comparative proteomic analysis of extracellular matrix proteins secreted by hypertrophic scar with normal skin fibroblasts.Burns & trauma · 2014Article
- Angiotensin II induces skin fibrosis: a novel mouse model of dermal fibrosis.Arthritis research & therapy · 2012Article
- A lipocalin-derived Peptide modulating fibroblasts and extracellular matrix proteins.Journal of toxicology · 2012Article
- Understanding fibrosis in systemic sclerosis: shifting paradigms, emerging opportunities.Nature reviews. Rheumatology · 2011Review
- Plasma and cellular fibronectin: distinct and independent functions during tissue repair.Fibrogenesis & tissue repair · 2011Article
- Cell-extracellular matrix interactions in normal and diseased skin.Cold Spring Harbor perspectives in biology · 2011Review
- Fibrosis in systemic sclerosis: emerging concepts and implications for targeted therapy.Autoimmunity reviews · 2011Article
- Characterization of monocyte/macrophage subsets in the skin and peripheral blood derived from patients with systemic sclerosis.Arthritis research & therapy · 2010Article
- Transcriptional regulation of matrix metalloproteinase-1 and collagen 1A2 explains the anti-fibrotic effect exerted by proteasome inhibition in human dermal fibroblasts.Arthritis research & therapy · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive extracellular matrix (ECM) deposition in the skin, lung, and other organs is a hallmark of systemic sclerosis (SSc). The pathogenesis of SSc is still poorly understood, but increasing evidence suggests that various cytokines such as transforming growth factor (TGF)-beta and their signaling pathways are key mediators of tissue fibrosis as a consequence of ECM accumulation in the pathogenesis of fibrosis such as SSc. TGF-beta regulates diverse biologic activities including cell growth, cell death or apoptosis, cell differentiation, and ECM synthesis. TGF-beta is known to induce the expression of ECM proteins in mesenchymal cells, and to stimulate the production of protease inhibitors that prevent enzymatic breakdown of the ECM. This paper focuses on the possible role of ECM, various cytokines, especially TGF-beta signal transduction pathways in the pathogenesis of fibrosis in SSc.
Indexed as
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.