ReviewRheumatology international2019
Interleukin-17 pathways in systemic sclerosis-associated fibrosis.
Review in Rheumatology international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 40 citations in OpenAlex.
- Emerging therapies for the treatment of systemic sclerosis.Nature reviews. Rheumatology · 2025Review
- Ferroptosis-related LncRNAs in diseases.BMC biology · 2025Review
- IL-17A mediates inflammation-related retinal pigment epithelial cells injuryInternational journal of ophthalmology · 2025Article
- Successful treatment of localized scleroderma using brodalumab: A case report.SAGE open medical case reports · 2025Article
- Single-cell RNA-seq reveals immune cell heterogeneity and increased Th17 cells in human fibrotic skin diseases.Frontiers in immunology · 2024Article
- The role of immune cells in the pathogenesis of connective tissue diseases-associated pulmonary arterial hypertension.Frontiers in immunology · 2024Review
- Article
- The Molecular Mechanisms of Systemic Sclerosis-Associated Lung Fibrosis.International journal of molecular sciences · 2023Review
- The role of heterodimer IL-17-A/F in atopic dermatitis.Postepy dermatologii i alergologii · 2022Article
- Plasma and Urine Levels of Glycosaminoglycans in Patients with Systemic Sclerosis and Their Relationship to Selected Interleukins and Marker of Early Kidney Injury.Journal of clinical medicine · 2022Article
- Research progress on drugs targeting the TGF-β signaling pathway in fibrotic diseases.Immunologic research · 2022Review
- Mechanisms of Xiaochaihu Decoction on Treating Hepatic Fibrosis Explored by Network Pharmacology.Disease markers · 2022Article
- Using Network Pharmacology to Explore the Mechanism of Panax notoginseng in the Treatment of Myocardial Fibrosis.Journal of diabetes research · 2022Article
- Management of Connective Tissue Disease-related Interstitial Lung Disease.Current pulmonology reports · 2022Review
- The Yin and Yang of IL-17 in Systemic Sclerosis.Frontiers in immunology · 2022Review
- 1,25OH-Vitamin D3 and IL-17 Inhibition Modulate Pro-Fibrotic Cytokines Production in Peripheral Blood Mononuclear Cells of Patients with Systemic Sclerosis.International journal of medical sciences · 2022Article
- Review
- Autoantibodies from Patients with Scleroderma Renal Crisis Promote PAR-1 Receptor Activation and IL-6 Production in Endothelial Cells.International journal of molecular sciences · 2021Article
- NETosis in Wound Healing: When Enough Is Enough.Cells · 2021Review
- Huangbai Liniment Ameliorates Skin Inflammation in Atopic Dermatitis.Frontiers in pharmacology · 2021Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis is unregulated tissue repair that may cause impairment of organ function, especially in end-organ damage. Systemic sclerosis (SSc) is the prototype systemic fibrosing disorder. Classical targets for fibrosis in SSc like transforming growth factor Beta (TGF-β), Interleukin-6 (IL-6), and multiple tyrosine kinases, have not yielded therapeutic benefit. There is multitude of evidence from across different tissues like the heart, lung, skin, liver, colon, and, to some extent, the kidney, that interleukin-17 (IL-17) and its downstream pathways are strongly associated with the initiation and propagation of fibrosis. Data from scleroderma patients, as well as from animal models of SSc, mirror these findings. Interestingly, hitherto unknown to be related to IL-17, newer molecules like Programmed Death-protein1 (PD-1), the phosphatase SHP2, along with known signal transducers like signal transducer and activator of transcription (STAT3), have been recently shown to be involved in the pathogenesis of fibrosis. Related molecules include the intracellular signalling molecules Ras/Erk, mammalian target organ of rapamycin (mTOR), and complement components. The biology of these pathways has not yet been fully elucidated to predict regulatory mechanisms, redundancies, and potential off-target effects. All these need to be better understood in the context of each other, in an effort to arrive at the optimal target to modulate fibrosis.
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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.