ArticleThe Journal of experimental medicine2014
Cardiac fibroblasts mediate IL-17A-driven inflammatory dilated cardiomyopathy.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.
- Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023Pooled it
- A narrative review of immune checkpoint inhibitor-related cardiotoxicity in lung cancer: mechanisms, risk stratification, and clinical management.Journal of thoracic disease · 2026Review
- IL-1-Activated Inflammatory Cardiac Fibroblasts Exacerbate Acute Coxsackievirus B3 Myocarditis.JACC. Basic to translational science · 2026Article
- The Immune System as a Proarrhythmic Mediator: A Novel Paradigm for the Development of New Antiarrhythmic Therapy.The Canadian journal of cardiology · 2026Review
- Macrophages of the heart: Homeostasis and disease.Biomedical journal · 2026Review
- Article
- TRIM21enhances IL-17A signaling and drives autoimmune myocarditis by promoting TRAF3 lysosomaldegradation in cardiac fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Interplay between IL-17 family members and angiogenic cytokines in subjects with systemic sclerosis.Archives of medical science : AMS · 2026Article
- Unsupervised feature extraction using deep learning empowers discovery of genetic determinants of the electrocardiogram.Genome medicine · 2025Article
- Fibroblast-Mediated Macrophage Recruitment Supports Acute Wound Healing.The Journal of investigative dermatology · 2025Article
- Effect of Continuous Lipopolysaccharide Induction on Oxidative Stress and Heart Injury in Weaned Piglets.Veterinary sciences · 2025Article
- Macrophage-derived SPP1 exacerbate myocardial injury by interacting with fibroblasts in viral myocarditis.Biology direct · 2025Article
- Cardiovascular adverse effects of immunotherapy in cancer: insights and implications.Frontiers in oncology · 2025Review
- The distinct functions of MIF in inflammatory cardiomyopathy.Frontiers in immunology · 2025Review
- Review
- Review
- Deep skin fibroblast-mediated macrophage recruitment supports acute wound healing.bioRxiv : the preprint server for biology · 2024Article
- Cardiac Fibroblastic Niches in Homeostasis and Inflammation.Circulation research · 2024Review
- Infectious factors in myocarditis: a comprehensive review of common and rare pathogens.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- Review
46 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
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Inflammatory dilated cardiomyopathy (DCMi) is a major cause of heart failure in individuals below the age of 40. We recently reported that IL-17A is required for the development of DCMi. We show a novel pathway connecting IL-17A, cardiac fibroblasts (CFs), GM-CSF, and heart-infiltrating myeloid cells with the pathogenesis of DCMi. Il17ra(-/-) mice were protected from DCMi, and this was associated with significantly diminished neutrophil and Ly6Chi monocyte/macrophage (MO/MΦ) cardiac infiltrates. Depletion of Ly6Chi MO/MΦ also protected mice from DCMi. Mechanistically, IL-17A stimulated CFs to produce key chemokines and cytokines that are critical downstream effectors in the recruitment and differentiation of myeloid cells. Moreover, IL-17A directs Ly6Chi MO/MΦ in trans toward a more proinflammatory phenotype via CF-derived GM-CSF. Collectively, this IL-17A-fibroblast-GM-CSF-MO/MΦ axis could provide a novel target for the treatment of DCMi and related inflammatory cardiac diseases.
Indexed as
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.