ReviewJournal of clinical medicine2023
Targeting Interleukin-17 as a Novel Treatment Option for Fibrotic Diseases.
Review in Journal of clinical medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 13 citations in OpenAlex.
- Hidradenitis suppurativa: epidemiology, diagnosis, molecular pathogenesis and therapy.Molecular biomedicine · 2026Review
- Transcriptomic identification of IL-17/FOS-associated signaling in dartos fascia remodeling of pediatric concealed penis.Frontiers in pediatrics · 2026Article
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- Engineered T cell therapy for the treatment of cardiac fibrosis during chronic phase of myocarditis.Theranostics · 2026Article
- Comprehensive Profiling of Cytokines and Growth Factors: Pathogenic Roles and Clinical Applications in Autoimmune Diseases.International journal of molecular sciences · 2025Review
- "The Ameliorative Effect of Interleukin-17A Neutralization on Doxorubicin-Induced Cardiotoxicity by Modulating the NF-κB/NLRP3/Caspase-1/IL-1β Signaling Pathway in Rats".Inflammation · 2025Article
- Endogenous Galectin-8 protects against Th17 infiltration and fibrosis following acute kidney injury.Molecular medicine (Cambridge, Mass.) · 2025Article
- Cardiac Fibrosis: Mechanistic Discoveries Linked to SGLT2 Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The mechanotransduction-immune axis in organ fibrosis: dual regulatory mechanisms and translational therapeutic perspectives.Frontiers in immunology · 2025Review
- IL-17 is associated with disease severity and targetable inflammatory processes in heart failure.ESC heart failure · 2024Article
- Novel Factors Regulating Proliferation, Migration, and Differentiation of Fibroblasts, Keratinocytes, and Vascular Smooth Muscle Cells during Wound Healing.Biomedicines · 2024Review
- Therapeutic targets for fibro-inflammation in Graves' orbitopathy.Taiwan journal of ophthalmologyReview
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis is the end result of persistent inflammatory responses induced by a variety of stimuli, including chronic infections, autoimmune reactions, and tissue injury. Fibrotic diseases affect all vital organs and are characterized by a high rate of morbidity and mortality in the developed world. Until recently, there were no approved antifibrotic therapies. In recent years, high levels of interleukin-17 (IL-17) have been associated with chronic inflammatory diseases with fibrotic complications that culminate in organ failure. In this review, we provide an update on the role of IL-17 in fibrotic diseases, with particular attention to the most recent lines of research in the therapeutic field represented by the epigenetic mechanisms that control IL-17 levels in fibrosis. A better knowledge of the IL-17 signaling pathway implications in fibrosis could design new strategies for therapeutic benefits.
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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.