ArticleFibrogenesis & tissue repair2012
Fibrosis in systemic sclerosis: common and unique pathobiology.
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 23 papers, 1 of them a synthesis that pooled it.
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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- The effect of TGF-β1 polymorphism on systemic sclerosis: a systematic review and pooled analysis of available literature.Rheumatology international · 2013Pooled it
- GRIM-19-mediated induction of mitochondrial STAT3 alleviates systemic sclerosis by inhibiting fibrosis and Th2/Th17 cells.Experimental & molecular medicine · 2024Article
- Nuclear IL-33 in Fibroblasts Promotes Skin Fibrosis.The Journal of investigative dermatology · 2023Article
- Therapeutic Options for Systemic Sclerosis: Current and Future Perspectives in Tackling Immune-Mediated Fibrosis.Biomedicines · 2022Review
- Role of adipokines in systemic sclerosis pathogenesis.European journal of rheumatology · 2020Review
- Role of Semaphorins in Immunopathologies and Rheumatic Diseases.International journal of molecular sciences · 2019Review
- Bufei Qingyu Granules Inhibit the Development of Systemic Sclerosis via Notch-1/Jagged-2 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Fibroproliferative genes are preferentially expressed in central centrifugal cicatricial alopecia.Journal of the American Academy of Dermatology · 2018Article
- Why target the tumor stroma in melanoma?Journal of cell communication and signaling · 2018Review
- Mesenchymal Stromal Cells Based Therapy in Systemic Sclerosis: Rational and Challenges.Frontiers in immunology · 2018Review
- Thermodynamic Aspects and Reprogramming Cellular Energy Metabolism during the Fibrosis Process.International journal of molecular sciences · 2017Review
- Interactions between TGF-β1, canonical WNT/β-catenin pathway and PPAR γ in radiation-induced fibrosis.Oncotarget · 2017Review
- Effectiveness of rosiglitazone in reducing flexion contracture in a rabbit model of arthrofibrosis with surgical capsular release: A biomechanical, histological, and genetic analysis.Bone & joint research · 2016Article
- Macitentan inhibits the transforming growth factor-β profibrotic action, blocking the signaling mediated by the ETR/TβRI complex in systemic sclerosis dermal fibroblasts.Arthritis research & therapy · 2015Article
- Gene expression profiling offers insights into the role of innate immune signaling in SSc.Seminars in immunopathology · 2015Review
- Genome-wide DNA methylation analysis in dermal fibroblasts from patients with diffuse and limited systemic sclerosis reveals common and subset-specific DNA methylation aberrancies.Annals of the rheumatic diseases · 2015Article
- MicroRNAs Regulating Signaling Pathways: Potential Biomarkers in Systemic Sclerosis.Genomics, proteomics & bioinformatics · 2015Review
- The Role of PPAR Gamma in Systemic Sclerosis.PPAR research · 2015Review
- Article
- Emerging roles of innate immune signaling and toll-like receptors in fibrosis and systemic sclerosis.Current rheumatology reports · 2015Review
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 at 1 institution in 1 country.
Funding
Abstract
Fibrosis in systemic sclerosis (SSc), a complex polygenic disease associated with autoimmunity and proliferative/obliterative vasculopathy, shares pathobiologic features in common with other fibrosing illnesses, but also has distinguishing characteristics. Fibroblast activation induced by transforming growth factor-β (TGF-β), Wnts and innate immune receptors, along with oxidative stress and reactive oxygen species (ROS) are implicated in pathogenesis. On the other hand, the roles of endothelial-mesenchymal differentiation and bone marrow-derived fibrocytes remain to be established. Fibrotic responses are modulated by transcriptional activators and cofactors, epigenetic factors, and microRNAs that can amplify or inhibit ligand-induced signaling. The nuclear orphan receptor PPAR-γ appears to be important in governing the duration and intensity of fibroblast activation and mesenchymal progenitor cell differentiation, and defects in PPAR-γ expression or function in SSc may underlie the uncontrolled progression of fibrosis. Identifying the perturbations in signaling pathways and cellular differentiation programs responsible for tissue damage and fibrosis in SSc allows their selective targeting using novel compounds, or by innovative uses of already-approved drugs (drug repurposing).
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.