ReviewCurrent opinion in rheumatology2015
Origin of fibrosing cells in systemic sclerosis.
Review in Current opinion in rheumatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 46 citations in OpenAlex.
- Role of Growth Factors in the Pathogenesis of Systemic-Sclerosis-Associated Fibrosis.International journal of molecular sciences · 2025Review
- Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025Review
- A review of recent studies on the pathogenesis of Systemic Sclerosis: focus on fibrosis pathways.Frontiers in immunology · 2025Review
- Tissue fibrosis associated depletion of lipid-filled cells.Experimental dermatology · 2024Review
- Article
- Cellular Transdifferentiation: A Crucial Mechanism of Fibrosis in Systemic Sclerosis.Current rheumatology reviews · 2024Review
- Immune and Non-Immune Inflammatory Cells Involved in Autoimmune Fibrosis: New Discoveries.Journal of clinical medicine · 2023Review
- SARA suppresses myofibroblast precursor transdifferentiation in fibrogenesis in a mouse model of scleroderma.JCI insight · 2022Article
- The compound LG283 inhibits bleomycin-induced skin fibrosis via antagonizing TGF-β signaling.Arthritis research & therapy · 2022Article
- Contributions of Immune Cells and Stromal Cells to the Pathogenesis of Systemic Sclerosis: Recent Insights.Frontiers in pharmacology · 2022Review
- Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021Review
- New Insights into Profibrotic Myofibroblast Formation in Systemic Sclerosis: When the Vascular Wall Becomes the Enemy.Life (Basel, Switzerland) · 2021Review
- Adipose-derived stem cells: Pathophysiologic implicationsWorld journal of stem cells · 2021Review
- The contribution of mesenchymal transitions to the pathogenesis of systemic sclerosis.European journal of rheumatology · 2020Review
- Extracellular SPARC cooperates with TGF-β signalling to induce pro-fibrotic activation of systemic sclerosis patient dermal fibroblasts.Rheumatology (Oxford, England) · 2020Article
- CD47 prevents the elimination of diseased fibroblasts in scleroderma.JCI insight · 2020Article
- Emerging Roles of Matricellular Proteins in Systemic Sclerosis.International journal of molecular sciences · 2020Review
- Pathogenic Roles of Autoantibodies and Aberrant Epigenetic Regulation of Immune and Connective Tissue Cells in the Tissue Fibrosis of Patients with Systemic Sclerosis.International journal of molecular sciences · 2020Review
- Review
- Induction of Inflammation and Fibrosis by Semaphorin 4A in Systemic Sclerosis.Arthritis & rheumatology (Hoboken, N.J.) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
purpose of reviewSystemic sclerosis, an autoimmune disease of unknown origin, is characterized by progressive fibrosis that can affect all organs of the body. To date, there are no effective therapies for the disease. This paucity of treatment options is primarily because of limited understanding of the processes that initiate and promote fibrosis in general and a lack of animal models that specifically emulate the chronic nature of systemic sclerosis. Most models capitulate acute injury-induced fibrosis in specific organs. Yet, regardless of the model a major outstanding question in the field is the cellular origin of fibrosing cells. RECENT
findingsA multitude of origins have been proposed in a variety of tissues, including resident tissue stroma, fibrocytes, pericytes, adipocytes, epithelial cells and endothelial cells. Developmentally derived fibroblast lineages have recently been elucidated with fibrosing potential in injury models. Increasing data support the pericyte as a fibrosing cell origin in diverse fibrosis models and adipocytes have recently been proposed. Fibrocytes, epithelial cells and endothelial cells also have been examined, although data do not as strongly support these possible origins. SUMMARY: In this review, we discuss recent evidence arguing in favor of and against proposed origins of fibrosing cells in diverse models of fibrosis. We highlight outstanding controversies and propose how future research may elucidate how fibrosing cells arise and what processes can be targeted in order to treat systemic sclerosis.
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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.