ReviewNature reviews. Rheumatology2011
Understanding fibrosis in systemic sclerosis: shifting paradigms, emerging opportunities.
Review in Nature reviews. Rheumatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 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
182 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Rituximab in systemic sclerosis-associated interstitial lung disease: A systematic review and meta-analysis.Science progressPooled it
- Interleukin-6 (IL-6) trans signaling drives a STAT3-dependent pathway that leads to hyperactive transforming growth factor-β (TGF-β) signaling promoting SMAD3 activation and fibrosis via Gremlin protein.The Journal of biological chemistry · 2014Trial
- Retrospective analysis of the frequency of centrofacial telangiectasia in systemic sclerosis patients treated with bosentan or ilomedin.European journal of medical research · 2014Trial
- Vitamin D Supplementation Modulates Base Excision Repair (BER) Machinery in Systemic Sclerosis: A Prospective Longitudinal Study.Biochemical genetics · 2026Article
- Reciprocal regulation of fibroblast-macrophage equilibrium governs skin integrity.Nature immunology · 2026Article
- Emerging Therapeutic Strategies for Nrf2-Associated Skin Disorders: From Photoaging to Autoimmunity.Antioxidants (Basel, Switzerland) · 2026Review
- An intricate relationship between fibrosis and autoimmune diseases: a specific focus on unraveling its molecular, immunological, and epigenetic drivers.Frontiers in immunology · 2026Review
- Soquelitinib inhibition of IL-2-inducible T cell kinase ameliorates lung damage in murine models of systemic sclerosis.Arthritis research & therapy · 2025Article
- Review
- Fibrotic Disease of the Skin and Lung: Shared Pathways, Environmental Drivers, and Therapeutic Opportunities in a Changing Climate.International journal of molecular sciences · 2025Review
- Silencing IFIT3 suppresses the EGFR/VEGF pathway and modulates SOCS1 to attenuate skin fibrosis in systemic sclerosis.Apoptosis : an international journal on programmed cell death · 2025Article
- The Role of Abatacept on Inflammation and Fibrosis in Hypochlorous Acid-Induced Fibrosis Mice.International journal of rheumatic diseases · 2025Article
- Aberrant Chitinase 3-Like 1 Expression in Basal Cells Contributes to Systemic Sclerosis Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The B-cells paradigm in systemic sclerosis: an update on pathophysiology and B-cell-targeted therapies.Clinical and experimental immunology · 2025Review
- Review
- Targeting CD13/Aminopeptidase N as a Novel Therapeutic Approach for Scleroderma Fibrosis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Review
- Inhibiting triggering receptor expressed on myeloid cells 1 signaling to ameliorate skin fibrosis.JCI insight · 2024Article
- Unraveling the role of MiR-181 in skin fibrosis pathogenesis by targeting NUDT21.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Extracellular Vesicles Derived from Adipose Stem Cells Alleviate Systemic Sclerosis by Inhibiting TGF-β Pathway.Biomolecules & therapeutics · 2024Article
122 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Fibrosis in multiple organs is a prominent pathological finding and distinguishing hallmark of systemic sclerosis (SSc). Findings during the past 5 years have contributed to a more complete understanding of the complex cellular and molecular underpinning of fibrosis in SSc. Fibroblasts, the principal effector cells, are activated in the profibrotic cellular milieu by cytokines and growth factors, developmental pathways, endothelin 1 and thrombin. Innate immune signaling via Toll-like receptors, matrix-generated biomechanical stress signaling via integrins, hypoxia and oxidative stress seem to be implicated in perpetuating the process. Beyond chronic fibroblast activation, fibrosis represents a failure to terminate tissue repair, coupled with an expanded population of mesenchymal cells originating from bone marrow and transdifferentiation of epithelial cells, endothelial cells and pericytes. In addition, studies have identified intrinsic alterations in SSc fibroblasts resulting from epigenetic changes, as well as altered microRNA expression that might underlie the cell-autonomous, persistent activation phenotype of these cells. Precise characterization of the deregulated extracellular and intracellular signaling pathways, mediators and cellular differentiation programs that contribute to fibrosis in SSc will facilitate the development of selective, targeted therapeutic strategies. Effective antifibrotic therapy will ultimately involve novel compounds and repurposing of drugs that are already approved for other indications.
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What Socratic 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 Socratic graph.