ArticleCardiovascular research2017
JAK-STAT signalling and the atrial fibrillation promoting fibrotic substrate.
Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed.
- Single-Nuclear RNA Sequencing Reveals Regional Specialization and Cellular Interactions in Epicardial and Perivascular Adipose Tissue.bioRxiv : the preprint server for biology · 2026Article
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- A titin truncating variant linked to atrial fibrillation increases atrial profibrotic signalling and cholinergic sensitivity.Cardiovascular research · 2026Article
- Unlocking the potential of mRNA nanomedicines for comprehensive fibrosis therapy.Molecular therapy. Nucleic acids · 2026Review
- ANGPTL2 and LTBP2: key mediators of inflammation and mitochondrial dysfunction in atrial fibrillation.Journal of cardiothoracic surgery · 2026Article
- Atrial fibrillation associated with tyrosine kinase inhibitors: A case-control study of real-world pharmacovigilance data.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Role ofInternational journal of molecular sciences · 2026Article
- Cellular and molecular cross-talk in atrial fibrillation: The role of non-cardiomyocytes in creating an arrhythmogenic substrate.The Journal of physiology · 2026Review
- Do nonsteroidal anti-inflammatory drugs increase the risk of atrial fibrillation after non-cardiac surgery? Insights from translational and clinical research.Journal of anesthesia, analgesia and critical care · 2025Review
- Reprogramming of Mitochondrial and Cellular Energy Metabolism in Fibroblasts and Cardiomyocytes: Mechanisms and Therapeutic Strategies in Cardiac Fibrosis.Journal of cardiovascular translational research · 2025Review
- Immune cells and arrhythmias.Cardiovascular research · 2025Review
- Translation of pathophysiological mechanisms of atrial fibrosis into new diagnostic and therapeutic approaches.Nature reviews. Cardiology · 2025Review
- Crip2 affects vascular development by fine-tuning endothelial cell aggregation and proliferation.Cellular and molecular life sciences : CMLS · 2025Article
- The role of miR-155 in cardiovascular diseases: Potential diagnostic and therapeutic targets.International journal of cardiology. Cardiovascular risk and prevention · 2025Review
- Differential risk of adverse drug reactions with baricitinib across age groups: integrating real-world pharmacovigilance and genetic causal inference.Therapeutic advances in drug safety · 2025Article
- Targeting inhibition of the inflammatory response: advances in the treatment of myocardial fibrosis with natural medicine and active ingredients.Frontiers in cardiovascular medicine · 2025Review
- Interactions between atrial fibrosis and inflammation in atrial fibrillation.Frontiers in cardiovascular medicine · 2025Review
- Platelet-derived Growth Factor Receptor-α Induces Contraction Knots and Inflammatory Pain-like Behavior in a Rat Model of Myofascial Trigger Points.Anesthesiology · 2024Article
- IGF2BP2-modified circular RNA circCHD7 promotes endometrial cancer progression via stabilizing PDGFRB and activating JAK/STAT signaling pathway.Cancer gene therapy · 2024Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsLeft-atrial (LA) fibrosis is an important feature of many atrial fibrillation (AF) substrates. The JAK-STAT system contributes to cardiac remodelling, but its role in AF is unknown. Here we investigated JAK-STAT changes in an AF-model and their potential contributions to LA-fibrosis. METHODS AND
resultsLA-remodelling was studied in dogs with heart failure (HF) induced by ventricular tachypacing (VTP, 240 bpm), and in mice with left-ventricular (LV) dysfunction due to myocardial infarction (MI). The selective STAT-3 inhibitor S3I-201 was administered to fibroblasts in vitro or mice in vivo (10 mg/kg/d, osmotic mini-pump). HF-dogs developed LA-selective fibrosis and AF-susceptibility at 1-week VTP. The mRNA-expression of platelet-derived growth factor (PDGF, a JAK-STAT activator) isoforms A, C and D, as well as JAK2, increased in LA fibroblasts from 1-week VTP. HF upregulated protein-expression of PDGF-receptor-β and phosphorylated (activated) signal transducer and activator of transcription 3 (STAT3) in LA. PDGF-AB stimulation of LA fibroblasts increased PDGFR-α, STAT3 and phosphorylated-STAT3 expression, as well as collagen-1 and fibronectin-1 protein secretion (by 1.6- to 20-fold), with smaller changes in LV fibroblasts. Phosphorylated-STAT3 and collagen upregulation were suppressed by the JAK2 inhibitor AG-490, PDGF receptor inhibitor AG1296 and STAT3-inhibitor SI3-201. In vivo S3I-201 treatment of MI-mice attenuated LA-fibrosis, LA-dilation and P-wave duration changes versus vehicle-control.
conclusionsHF activates the LA JAK-STAT system and enhances PDGF-signalling. JAK-STAT inhibition reduces the profibrotic effects of PDGF stimulation on canine fibroblasts in vitro while attenuating in vivo LA-fibrosis and remodelling in post-MI mice, suggesting that the JAK/STAT pathway contributes to LA-fibrogenesis and might be a potential target for LA-fibrosis prevention.
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Registered trials
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